ID	NAME	CLASS	GENES	DISEASES	DRUGS	DESCRIPTION
hsa04614	Renin-angiotensin system - Homo sapiens (human)	Organismal Systems; Endocrine System	183:AGT|5972:REN|1636:ACE|59272:ACE2|1215:CMA1|1511:CTSG|2028:ENPEP|290:ANPEP|5476:CTSA|1359:CPA3|4311:MME|7064:THOP1|57486:NLN|4142:MAS1|185:AGTR1|186:AGTR2|4012:LNPEP	Uromodulin-associated kidney diseases|Renal tubular dysgenesis	Captopril (JP16/USP/INN)|Losartan potassium (JP16/USAN)|Lisinopril hydrate (JP16)|Trandolapril (JAN/INN)|Valsartan (JAN/USAN/INN)|Ramipril (USP/INN)|Quinapril hydrochloride (JP16/USP)|Candesartan (USAN/INN)|Irbesartan (JAN/USAN/INN)|Benazepril hydrochloride (JAN/USAN)|Enalapril maleate (JP16/USP)|Fosinopril sodium (USAN)|Moexipril hydrochloride (USAN)|Perindopril erbumine (JAN/USAN)|Candesartan cilexetil (JP16/USAN)|Telmisartan (JAN/USAN/INN)|Cilazapril hydrate (JP16)|Candoxatril (JAN/USAN/INN)|Temocapril hydrochloride (JP16/USAN)|Olmesartan medoxomil (JAN/USAN)|Imidapril hydrochloride (JP16)|Delapril hydrochloride (JAN/USAN)|Alacepril (JP16/INN)|Eprosartan mesylate (USAN)|Benazeprilat (USAN/INN)|Aliskiren (USAN/INN)|Candoxatrilat (USAN/INN)|Ceronapril (USAN/INN)|Enalkiren (USAN/INN)|Ditekiren (USAN)|Terlakiren (USAN/INN)|Zankiren hydrochloride (USAN)|Quinapril (USP/INN)|Perindopril (USAN/INN)|Indolapril hydrochloride (USAN)|Libenzapril (USAN/INN)|Pentopril (USAN/INN)|Pivopril (USAN/INN)|Spirapril hydrochloride (USAN)|Zofenopril calcium (USAN)|Enalaprilat (USP)|Fosinoprilat (USAN/INN)|Quinaprilat (USAN/INN)|Spiraprilat (USAN/INN)|Zofenoprilat arginine (USAN)|Ecadotril (USAN/INN)|Eprosartan (USAN/INN)|Saralasin acetate (USAN)|Forasartan (USAN/INN)|Olmesartan (USAN/INN)|Teprotide (USAN/INN)|Aliskiren fumarate (JAN/USAN)|Benazepril (INN)|Cilazapril (INN)|Delapril  (INN)|Enalapril (INN)|Fosinopril (INN)|Azilsartan medoxomil (USAN)|Imidapril (INN)|Lisinopril (INN)|Losartan (INN)|Temocapril (INN)|Zofenopril (INN)|Azilsartan (JAN/USAN/INN)|Remikiren (INN)	
hsa04810	Regulation of actin cytoskeleton - Homo sapiens (human)	Cellular Processes; Cell Motility	2147:F2|2149:F2R|929:CD14|3630:INS|1950:EGF|2258:FGF13|2253:FGF8|8817:FGF18|2257:FGF12|2248:FGF3|2251:FGF6|2256:FGF11|8823:FGF16|2252:FGF7|2259:FGF14|8822:FGF17|9965:FGF19|2254:FGF9|2250:FGF5|2249:FGF4|8074:FGF23|27006:FGF22|26281:FGF20|2255:FGF10|2247:FGF2|26291:FGF21|2246:FGF1|5154:PDGFA|5155:PDGFB|56034:PDGFC|80310:PDGFD|3645:INSRR|1956:EGFR|2260:FGFR1|2263:FGFR2|2261:FGFR3|2264:FGFR4|5156:PDGFRA|5159:PDGFRB|2335:FN1|3672:ITGA1|3673:ITGA2|3674:ITGA2B|3675:ITGA3|3676:ITGA4|3678:ITGA5|3655:ITGA6|3679:ITGA7|8516:ITGA8|3680:ITGA9|8515:ITGA10|22801:ITGA11|3685:ITGAV|3683:ITGAL|3684:ITGAM|3687:ITGAX|3681:ITGAD|3682:ITGAE|3688:ITGB1|3689:ITGB2|3690:ITGB3|3691:ITGB4|3693:ITGB5|3694:ITGB6|3695:ITGB7|3696:ITGB8|623:BDKRB1|624:BDKRB2|1128:CHRM1|1129:CHRM2|1131:CHRM3|1132:CHRM4|1133:CHRM5|2768:GNA12|10672:GNA13|55970:GNG12|2245:FGD1|89846:FGD3|5747:PTK2|9564:BCAR1|1399:CRKL|1398:CRK|1793:DOCK1|6714:SRC|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|6237:RRAS|22800:RRAS2|22808:MRAS|9459:ARHGEF6|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|10451:VAV3|7409:VAV1|7410:VAV2|26230:TIAM2|7074:TIAM1|369:ARAF|673:BRAF|5894:RAF1|4342:MOS|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|9138:ARHGEF1|23365:ARHGEF12|2909:ARHGAP35|387:RHOA|5879:RAC1|5880:RAC2|5881:RAC3|998:CDC42|5058:PAK1|5062:PAK2|5063:PAK3|10298:PAK4|56924:PAK6|57144:PAK7|8874:ARHGEF7|28964:GIT1|6093:ROCK1|9475:ROCK2|4638:MYLK|85366:MYLK2|91807:MYLK3|5501:PPP1CC|5499:PPP1CA|5500:PPP1CB|4659:PPP1R12A|4633:MYL2|4636:MYL5|58498:MYL7|10398:MYL9|93408:MYL10|10627:MYL12A|103910:MYL12B|29895:MYLPF|1729:DIAPH1|1730:DIAPH2|6548:SLC9A1|8394:PIP5K1A|8395:PIP5K1B|23396:PIP5K1C|5305:PIP4K2A|8396:PIP4K2B|79837:PIP4K2C|200576:PIKFYVE|3984:LIMK1|3985:LIMK2|81624:DIAPH3|10458:BAIAP2|55740:ENAH|7454:WAS|8976:WASL|10163:WASF2|26999:CYFIP2|23191:CYFIP1|3071:NCKAP1L|10787:NCKAP1|10152:ABI2|55845:BRK1|8936:WASF1|10092:ARPC5|81873:ARPC5L|10093:ARPC4|10094:ARPC3|10095:ARPC1B|10552:ARPC1A|10109:ARPC2|60:ACTB|71:ACTG1|375189:PFN4|5217:PFN2|5216:PFN1|345456:PFN3|5829:PXN|7430:EZR|5962:RDX|4478:MSN|9087:TMSB4Y|7114:TMSB4X|1072:CFL1|1073:CFL2|54961:SSH3|85464:SSH2|54434:SSH1|7414:VCL|10788:IQGAP2|128239:IQGAP3|8826:IQGAP1|2934:GSN|85477:SCIN|81:ACTN4|88:ACTN2|87:ACTN1|89:ACTN3|10297:APC2|324:APC|50649:ARHGEF4|4627:MYH9|4628:MYH10|79784:MYH14	Non-syndromic X-linked mental retardation|Aarskog-Scott syndrome|MYH9-related kidney diseases|Epidermolysis bullosa, junctional|Congenital muscular dystrophies (CMD/MDC)|Nephrotic syndrome and focal segmental glomerulosclerosis|Lacrimo-auriculo-dento-digital syndrome (LADD)|Nemaline myopathy|Familial thoracic aortic aneurysm and dissection (TAAD)|Familial amyloidosis|Lethal congenital contractural syndrome (LCCS)|Lattice corneal dystrophies (LCD)|Fleck corneal dystrophy (FCD)|CATSHL syndrome|Familial adenomatous polyposis|Familial tumoral calcinosis (FTC)|Trigonocephaly	Thrombin (JP16/USP/INN)|Atropine (USP)|Scopolamine (INN)|Argatroban hydrate (JP16)|Pilocarpine (JAN/USP)|Fasudil hydrochloride (JAN)|Ximelagatran (JAN/USAN/INN)|Pilocarpine hydrochloride (JP16/USP)|Becaplermin (USAN/INN)|Fasudil hydrochloride hydrate (JAN)|Bivalirudin (USAN/INN)|Desirudin (USAN/INN)|Efegatran sulfate (USAN)|Napsagatran (USAN)|Efalizumab (USAN/INN)|Icatibant acetate (USAN)|Pilocarpine nitrate (USP)|Lepirudin (INN)|Dabigatran etexilate methanesulfonate (JAN)|Melagatran (INN)|Fasudil (INN)|Valategrast hydrochloride (USAN)	
hsa04150	mTOR signaling pathway - Homo sapiens (human)	Environmental Information Processing; Signal Transduction	3630:INS|3479:IGF1|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|5170:PDPK1|207:AKT1|208:AKT2|10000:AKT3|7248:TSC1|7249:TSC2|6009:RHEB|64223:MLST8|2475:MTOR|57521:RPTOR|253260:RICTOR|3091:HIF1A|7423:VEGFB|5228:PGF|7422:VEGFA|7424:VEGFC|2277:FIGF|6199:RPS6KB2|6198:RPS6KB1|1975:EIF4B|6194:RPS6|1978:EIF4EBP1|9470:EIF4E2|1977:EIF4E|253314:EIF4E1B|8408:ULK1|25989:ULK3|9706:ULK2|5594:MAPK1|5595:MAPK3|6195:RPS6KA1|6196:RPS6KA2|6197:RPS6KA3|27330:RPS6KA6|54541:DDIT4|6794:STK11|92335:STRADA|51719:CAB39|81617:CAB39L|5562:PRKAA1|5563:PRKAA2|673:BRAF	PTEN hamartoma tumor syndrome (PHTS)|Peutz-Jeghers syndrome|Lymphangioleiomyomatosis (LAM)|Tuberous sclerosis complex (TSC)|Polyhydramnios, megalencephaly, and symptomatic epilepsy	Buformin (USAN/INN)|Sirolimus (USAN/INN)|Metformin hydrochloride (JP16/USP)|Buformin hydrochloride (JP16)|Everolimus (JAN/USAN/INN)|Dapiclermin (USAN/INN)|Metformin (USAN/INN)|Temsirolimus (JAN/USAN/INN)|Sorafenib tosilate (JAN)|Bevacizumab (genetical recombination) (JAN)|Sorafenib (USAN/INN)	
hsa00592	alpha-Linolenic acid metabolism - Homo sapiens (human)	Metabolism; Lipid Metabolism	391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|151056:PLB1|9415:FADS2|8310:ACOX3|51:ACOX1|30:ACAA1	Peroxisomal beta-oxidation enzyme deficiency		
hsa00052	Galactose metabolism - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	2585:GALK2|2584:GALK1|2582:GALE|7360:UGP2|5236:PGM1|55276:PGM2|3101:HK3|3099:HK2|3098:HK1|80201:HKDC1|2645:GCK|2538:G6PC|57818:G6PC2|2720:GLB1|3938:LCT|3906:LALBA|2683:B4GALT1|8704:B4GALT2|2592:GALT|2717:GLA|231:AKR1B1|5214:PFKP|5211:PFKL|5213:PFKM|8972:MGAM|2548:GAA|2595:GANC|6476:SI|57016:AKR1B10	Galactosemia|Congenital lactase deficiency	Acarbose (JAN/USAN/INN)|Miglitol (JAN/USAN/INN)|Voglibose (JP16/USAN/INN)	
hsa00290	Valine, leucine and isoleucine biosynthesis - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	586:BCAT1|587:BCAT2|5160:PDHA1|5161:PDHA2|5162:PDHB			
hsa00240	Pyrimidine metabolism - Homo sapiens (human)	Metabolism; Nucleotide Metabolism	790:CAD|1723:DHODH|7372:UMPS|51727:CMPK1|129607:CMPK2|50808:AK3|8382:NME5|4832:NME3|4830:NME1|10201:NME6|4833:NME4|29922:NME7|654364:NME1-NME2|4831:NME2|87178:PNPT1|377841:ENTPD8|956:ENTPD3|953:ENTPD1|124583:CANT1|9583:ENTPD4|957:ENTPD5|955:ENTPD6|3704:ITPA|1503:CTPS|56474:CTPS2|25885:POLR1A|84172:POLR1B|30834:ZNRD1|221830:TWISTNB|64425:POLR1E|5430:POLR2A|5431:POLR2B|5432:POLR2C|5433:POLR2D|5434:POLR2E|5435:POLR2F|5436:POLR2G|5437:POLR2H|5438:POLR2I|5441:POLR2L|5439:POLR2J|246721:POLR2J2|548644:POLR2J3|5440:POLR2K|11128:POLR3A|55703:POLR3B|10623:POLR3C|661:POLR3D|55718:POLR3E|9533:POLR1C|51728:POLR3K|51082:POLR1D|171568:POLR3H|10622:POLR3G|84265:POLR3GL|10621:POLR3F|5422:POLA1|23649:POLA2|5557:PRIM1|5558:PRIM2|5424:POLD1|5425:POLD2|10714:POLD3|57804:POLD4|5426:POLE|5427:POLE2|54107:POLE3|56655:POLE4|54963:UCKL1|7371:UCK2|83549:UCK1|4907:NT5E|22978:NT5C2|51251:NT5C3|56953:NT5M|30833:NT5C|93034:NT5C1B|84618:NT5C1A|151531:UPP2|7378:UPP1|139596:UPRT|1806:DPYD|1807:DPYS|51733:UPB1|114112:TXNRD3|10587:TXNRD2|7296:TXNRD1|6240:RRM1|6241:RRM2|50484:RRM2B|1854:DUT|7298:TYMS|978:CDA|1890:TYMP|4860:PNP|1633:DCK|1635:DCTD|7084:TK2|7083:TK1|1841:DTYMK|318:NUDT2	Dihydropyrimidine dehydrogenase deficiency|Orotic aciduria|Dihydropyrimidinase deficiency|Beta-ureidopropionase deficiency|Mitochondrial DNA depletion syndrome (MDS)|Desbuquois syndrome|Anemia due to disorders of nucleotide metabolism|Calcification of joints and arteries|Progressive external ophthalmoplegia (PEO)	Hydroxycarbamide (JAN/INN)|Fluorouracil (JP16/USP/INN)|Leflunomide (JAN/USAN/INN)|Raltitrexed (JAN/USAN/INN)|Gemcitabine hydrochloride (JAN/USAN)|Capecitabine (JAN/USAN/INN)|Tegafur (JP16/USAN/INN)|Doxifluridine (JP16/INN)|Carmofur (JP16/INN)|Gimeracil (JAN/INN)|Tegafur - uracil mixt|Gemcitabine (USAN/INN)|Brequinar sodium (USAN)|Pemetrexed disodium (USAN)|Floxuridine (USP/INN)|Forodesine hydrochloride (JAN/USAN)|Metesind glucuronate (USAN)|Pemetrexed sodium hydrate (JAN)|Forodesine (USAN/INN)|Pemetrexed (INN)|Allopurinol sodium|Fluorouracil sodium salt	
hsa00061	Fatty acid biosynthesis - Homo sapiens (human)	Metabolism; Lipid Metabolism	31:ACACA|32:ACACB|27349:MCAT|2194:FASN|54995:OXSM|55301:OLAH			
hsa00750	Vitamin B6 metabolism - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	55163:PNPO|8566:PDXK|57026:PDXP|493911:PHOSPHO2|316:AOX1|29968:PSAT1	Phosphoserine aminotransferase (PSAT) deficiency|Pyridox(am)ine-5'-phosphate oxidase (PNPO) deficiency		
hsa04912	GnRH signaling pathway - Homo sapiens (human)	Organismal Systems; Endocrine System	2796:GNRH1|2797:GNRH2|2798:GNRHR|2778:GNAS|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|468:ATF4|2776:GNAQ|2767:GNA11|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|3708:ITPR1|3709:ITPR2|3710:ITPR3|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|4214:MAP3K1|10746:MAP3K2|4215:MAP3K3|4216:MAP3K4|5606:MAP2K3|5608:MAP2K6|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|5598:MAPK7|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|5337:PLD1|5338:PLD2|6714:SRC|998:CDC42|6416:MAP2K4|5609:MAP2K7|5602:MAPK10|5601:MAPK9|5599:MAPK8|3725:JUN|3972:LHB|1081:CGA|2488:FSHB|2185:PTK2B|4313:MMP2|4323:MMP14|1839:HBEGF|1956:EGFR|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|2002:ELK1|5578:PRKCA|5579:PRKCB|5580:PRKCD	Hypokalemic periodic paralysis (HypoPP)|Precocious puberty	Goserelin acetate (JAN)|Gonadorelin hydrochloride (USP)|Leuprorelin acetate (JAN)|Nafarelin acetate (JAN/USAN)|Cetrorelix acetate (JAN/USAN)|Buserelin acetate (JAN/USAN)|Histrelin acetate|Histrelin (USAN/INN)|Abarelix (USAN/INN)|Batimastat (USAN/INN)|Gonadorelin diacetate (JP16)|Detirelix acetate (USAN)|Ganirelix acetate (JAN/USAN)|Gonadorelin acetate (USAN)|Goserelin (USAN/INN)|Iturelix (USAN/INN)|Triptorelin (USAN/INN)|Triptorelin pamoate (USAN)|Buserelin (INN)|Cetrorelix (INN)|Ganirelix (INN)|Gonadorelin (INN)|Leuprorelin (INN)|Nafarelin (INN)|Degarelix acetate (USAN)|Triptorelin acetate|Degarelix (INN/USAN)|Degarelix acetate (JAN)	Gonadotropin-releasing hormone (GnRH) secretion from the hypothalamus acts upon its receptor in the anterior pituitary to regulate the production and release of the gonadotropins, LH and FSH. The GnRHR is coupled to Gq/11 proteins to activate phospholipase C which transmits its signal to diacylglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3). DAG activates the intracellular protein kinase C (PKC) pathway and IP3 stimulates release of intracellular calcium. In addition to the classical Gq/11, coupling of Gs is occasionally observed in a cell-specific fashion. Signaling downstream of protein kinase C (PKC) leads to transactivation of the epidermal growth factor (EGF) receptor and activation of mitogen-activated protein kinases (MAPKs), including extracellular-signal-regulated kinase (ERK), Jun N-terminal kinase (JNK) and p38 MAPK. Active MAPKs translocate to the nucleus, resulting in activation of transcription factors and rapid induction of early genes.
hsa03008	Ribosome biogenesis in eukaryotes - Homo sapiens (human)	Genetic Information Processing; Translation	1460:CSNK2B|1459:CSNK2A2|1457:CSNK2A1|65083:NOL6|27341:RRP7A|23160:WDR43|84916:CIRH1A|84135:UTP15|55127:HEATR1|84128:WDR75|51096:UTP18|134430:WDR36|10607:TBL3|10885:WDR3|55813:UTP6|5822:PWP2|10199:MPHOSPH10|55272:IMP3|92856:IMP4|6949:TCOF1|2091:FBL|10528:NOP56|51602:NOP58|4809:NHP2L1|1736:DKC1|55651:NHP2|54433:GAR1|55505:NOP10|51077:FCF1|9724:UTP14C|10813:UTP14A|29102:DROSHA|10436:EMG1|9790:BMS1|55226:NAT10|10171:RCL1|10940:POP1|10557:RPP38|10775:POP4|51367:POP5|54913:RPP25|138716:RPP25L|10248:POP7|10556:RPP30|10799:RPP40|254958:REXO1L1|100288562:exonuclease|57455:REXO1|25996:REXO2|54464:XRN1|22803:XRN2|23560:GTPBP4|29889:GNL2|54552:GNL3L|26354:GNL3|4931:NVL|23195:MDN1|55131:RBM28|28987:NOB1|5901:RAN|7514:XPO1|51068:NMD3|55998:NXF5|56000:NXF3|56001:NXF2|10482:NXF1|728343:NXF2B|55916:NXT2|29107:NXT1|3692:EIF6|51119:SBDS|79631:EFTUD1|55341:LSG1|166378:SPATA5|6880:TAF9|83732:RIOK1|55781:RIOK2|4549:RNR1|4550:RNR2	Spinocerebellar ataxia (SCA)|Shwachman-Diamond syndrome (SDS)|Dyskeratosis congenita (DC)|RMRP related disorders|Treacher Collins syndrome|Primary open angle glaucoma|Bowen-Conradi syndrome (BCS)|Alopecia neurologic defects and endocrinopathy syndrome (ANE syndrome)|Familial cholestasis|Hoyeraal-Hreidarsson syndrome		Ribosomes are the cellular factories responsible for making proteins. In eukaryotes, ribosome biogenesis involves the production and correct assembly of four rRNAs and about 80 ribosomal proteins. It requires hundreds of factors not present in the mature particle. In the absence of these proteins, ribosome biogenesis is stalled and cell growth is terminated even under optimal growth conditions. The primary pre-rRNA transcript is  assembled into the 90S pre-ribosome, which contains both 40S and 60S assembly factors. Within this complex, the pre-rRNA is cleaved. pre-60S ribosomes are subjected to several sequential processing steps in the nucleoplasm involving numerous assembly intermediates before it is exported to the cytoplasm and matured into the 60S ribosomal subunit. The pre-40S ribosome is matured to the small ribosomal subunit in the cytoplasm by cleavage.
hsa00010	Glycolysis / Gluconeogenesis - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	3101:HK3|3099:HK2|3098:HK1|80201:HKDC1|2645:GCK|2821:GPI|5214:PFKP|5211:PFKL|5213:PFKM|8789:FBP2|2203:FBP1|229:ALDOB|230:ALDOC|226:ALDOA|7167:TPI1|2597:GAPDH|26330:GAPDHS|5232:PGK2|5230:PGK1|5224:PGAM2|5223:PGAM1|441531:PGAM4|2027:ENO3|2026:ENO2|2023:ENO1|5315:PKM2|5313:PKLR|5160:PDHA1|5161:PDHA2|5162:PDHB|1737:DLAT|1738:DLD|92483:LDHAL6B|3948:LDHC|3939:LDHA|160287:LDHAL6A|3945:LDHB|126:ADH1C|131:ADH7|124:ADH1A|125:ADH1B|127:ADH4|128:ADH5|130:ADH6|10327:AKR1A1|219:ALDH1B1|224:ALDH3A2|217:ALDH2|501:ALDH7A1|223:ALDH9A1|222:ALDH3B2|220:ALDH1A3|221:ALDH3B1|218:ALDH3A1|55902:ACSS2|84532:ACSS1|130589:GALM|5236:PGM1|55276:PGM2|2538:G6PC|57818:G6PC2|83440:ADPGK|669:BPGM|5106:PCK2|5105:PCK1	Hereditary fructose intolerance|Pyruvate dehydrogenase complex deficiency|Fructose-1,6-bisphosphatase deficiency|Anemia due to disorders of glycolytic enzymes|Acute alcohol sensitivity|Pyruvate kinase (PK) deficiency	Cyanamide (JP16)|Disulfiram (JP16/USP/INN)|Fomepizole (USAN/INN)	Glycolysis is the process of converting glucose into pyruvate and generating small amounts of ATP (energy) and NADH (reducing power). It is a central pathway that produces important precursor metabolites: six-carbon compounds of glucose-6P and fructose-6P and three-carbon compounds of glycerone-P, glyceraldehyde-3P, glycerate-3P, phosphoenolpyruvate, and pyruvate [MD:M00001]. Acetyl-CoA, another important precursor metabolite, is produced by oxidative decarboxylation of pyruvate [MD:M00307]. When the enzyme genes of this pathway are examined in completely sequenced genomes, the reaction steps of three-carbon compounds from glycerone-P to pyruvate form a conserved core module [MD:M00002], which is found in almost all organisms and which often corresponds to operon structures in bacterial genomes. Gluconeogenesis is a synthesis pathway of glucose from noncarbohydrate precursors. It is essentially a reversal of glycolysis with minor variations of alternative paths [MD:M00003].
hsa04640	Hematopoietic cell lineage - Homo sapiens (human)	Organismal Systems; Immune System	4254:KITLG|3574:IL7|3565:IL4|1437:CSF2|2323:FLT3LG|3567:IL5|1440:CSF3|3562:IL3|3569:IL6|3589:IL11|3552:IL1A|3553:IL1B|7124:TNF|1435:CSF1|2056:EPO|7173:TPO|7066:THPO|947:CD34|2322:FLT3|1791:DNTT|960:CD44|3815:KIT|3559:IL2RA|3575:IL7R|7037:TFRC|924:CD7|914:CD2|921:CD5|909:CD1A|910:CD1B|911:CD1C|913:CD1E|912:CD1D|920:CD4|925:CD8A|926:CD8B|915:CD3D|916:CD3E|917:CD3G|4311:MME|928:CD9|930:CD19|933:CD22|100133941:CD24|931:MS4A1|1380:CR2|951:CD37|100132941:uncharacterized|100291917:uncharacterized|2208:FCER2|1378:CR1|1438:CSF2RA|3563:IL3RA|945:CD33|3566:IL4R|3570:IL6R|2209:FCGR1A|1436:CSF1R|290:ANPEP|3684:ITGAM|929:CD14|3581:IL9R|3554:IL1R1|7850:IL1R2|1441:CSF3R|3568:IL5RA|2057:EPOR|948:CD36|1604:CD55|966:CD59|3590:IL11RA|3690:ITGB3|3674:ITGA2B|2815:GP9|2811:GP1BA|2812:GP1BB|2814:GP5|3672:ITGA1|3673:ITGA2|3675:ITGA3|3676:ITGA4|3678:ITGA5|3655:ITGA6|2993:GYPA|3122:HLA-DRA|3123:HLA-DRB1|3125:HLA-DRB3|3126:HLA-DRB4|3127:HLA-DRB5|952:CD38	Hemophilia|Bernard-Soulier syndrome	Imatinib mesilate (JAN)|Tocilizumab (genetical recombination) (JAN)|Rituximab (genetical recombination) (JAN)|Basiliximab (genetical recombination) (JAN)|Epoetin alfa (genetical recombination) (JAN)|Epoetin beta (genetical recombination) (JAN)|Gemtuzumab ozogamicin (genetical recombination) (JAN)|Daclizumab (USAN/INN)|Daniplestim (USAN/INN)|Darbepoetin alfa (genetical recombination) (JAN)|Epoetin delta (USAN)|Epratuzumab (USAN/INN)|Ibritumomab tiuxetan (genetical recombination) (JAN)|Muromonab-CD3 (JAN/USAN/INN)|Ocrelizumab (genetical recombination) (JAN)|Siplizumab (USAN/INN)|Lumiliximab (USAN/INN)|Imatinib (INN)|Tositumomab (INN)|Tositumomab 131 iodine|Catumaxomab (INN)|Ofatumumab (genetical recombination) (JAN)|Valategrast hydrochloride (USAN)	Blood-cell development progresses from a hematopoietic stem cell (HSC), which can undergo either self-renewal or differentiation into a multilineage committed progenitor cell: a common lymphoid progenitor (CLP) or a common myeloid progenitor (CMP). A CLP gives rise to the lymphoid lineage of white blood cells or leukocytes-the natural killer (NK) cells and the T and B lymphocytes. A CMP gives rise to the myeloid lineage, which comprises the rest of the leukocytes, the erythrocytes (red blood cells), and the megakaryocytes that produce platelets important in blood clotting. Cells undergoing these differentiation process express a stage- and lineage-specific set of surface markers. Therefore cellular stages are identified by the specific expression patterns of these genes.
hsa04080	Neuroactive ligand-receptor interaction - Homo sapiens (human)	Environmental Information Processing; Signaling Molecules and Interaction	1128:CHRM1|1129:CHRM2|1131:CHRM3|1132:CHRM4|1133:CHRM5|148:ADRA1A|147:ADRA1B|146:ADRA1D|150:ADRA2A|151:ADRA2B|152:ADRA2C|153:ADRB1|154:ADRB2|155:ADRB3|1812:DRD1|1813:DRD2|1814:DRD3|1815:DRD4|1816:DRD5|3269:HRH1|3274:HRH2|11255:HRH3|59340:HRH4|3355:HTR1F|3354:HTR1E|3351:HTR1B|3352:HTR1D|3350:HTR1A|3358:HTR2C|3357:HTR2B|3356:HTR2A|3360:HTR4|3361:HTR5A|3362:HTR6|3363:HTR7|9287:TAAR2|9038:TAAR5|83551:TAAR8|134864:TAAR1|134860:TAAR9|319100:TAAR6|185:AGTR1|186:AGTR2|4829:NMBR|2925:GRPR|680:BRS3|623:BDKRB1|624:BDKRB2|728:C5AR1|719:C3AR1|2357:FPR1|2359:FPR3|2358:FPR2|187:APLNR|886:CCKAR|887:CCKBR|1909:EDNRA|1910:EDNRB|4157:MC1R|4158:MC2R|4159:MC3R|4160:MC4R|4161:MC5R|5540:PPYR1|4886:NPY1R|4887:NPY2R|4889:NPY5R|10888:GPR83|4923:NTSR1|23620:NTSR2|4985:OPRD1|4986:OPRK1|4988:OPRM1|4987:OPRL1|6751:SSTR1|6752:SSTR2|6753:SSTR3|6754:SSTR4|6755:SSTR5|6869:TACR1|6865:TACR2|6870:TACR3|552:AVPR1A|553:AVPR1B|554:AVPR2|5021:OXTR|2587:GALR1|8811:GALR2|8484:GALR3|2147:F2|1511:CTSG|3001:GZMA|5340:PLG|5646:PRSS3|5645:PRSS2|5644:PRSS1|2149:F2R|2150:F2RL1|2151:F2RL2|9002:F2RL3|56288:PARD3|3061:HCRTR1|3062:HCRTR2|64106:NPFFR1|10886:NPFFR2|2837:UTS2R|10316:NMUR1|56923:NMUR2|2847:MCHR1|84539:MCHR2|2488:FSHB|2492:FSHR|7252:TSHB|3973:LHCGR|7253:TSHR|5729:PTGDR|5731:PTGER1|5732:PTGER2|5733:PTGER3|5734:PTGER4|5737:PTGFR|5739:PTGIR|6915:TBXA2R|134:ADORA1|135:ADORA2A|136:ADORA2B|140:ADORA3|5029:P2RY2|5028:P2RY1|5030:P2RY4|5031:P2RY6|10161:LPAR6|27334:P2RY10|9934:P2RY14|286530:P2RY8|5032:P2RY11|53829:P2RY13|2846:LPAR4|2859:GPR35|1268:CNR1|1269:CNR2|5724:PTAFR|2798:GNRHR|7201:TRHR|2693:GHSR|84634:KISS1R|4543:MTNR1A|4544:MTNR1B|9248:GPR50|1901:S1PR1|1902:LPAR1|1903:S1PR3|9170:LPAR2|9294:S1PR2|8698:S1PR4|23566:LPAR3|53637:S1PR5|1241:LTB4R|56413:LTB4R2|4142:MAS1|59350:RXFP1|122042:RXFP2|10800:CYSLTR1|57105:CYSLTR2|799:CALCR|10203:CALCRL|1394:CRHR1|1395:CRHR2|2696:GIPR|2740:GLP1R|9340:GLP2R|2642:GCGR|2692:GHRHR|5745:PTH1R|5746:PTH2R|117:ADCYAP1R1|6344:SCTR|7433:VIPR1|7434:VIPR2|2911:GRM1|2915:GRM5|2912:GRM2|2913:GRM3|2914:GRM4|2916:GRM6|2918:GRM8|2917:GRM7|9568:GABBR2|2550:GABBR1|165829:GPR156|2862:MLNR|2831:NPBWR1|2832:NPBWR2|2834:PRLHR|2902:GRIN1|2903:GRIN2A|2904:GRIN2B|2905:GRIN2C|2906:GRIN2D|116443:GRIN3A|116444:GRIN3B|2555:GABRA2|2554:GABRA1|2557:GABRA4|2556:GABRA3|2558:GABRA5|2559:GABRA6|2560:GABRB1|2562:GABRB3|2561:GABRB2|2563:GABRD|2564:GABRE|2566:GABRG2|2565:GABRG1|2567:GABRG3|2568:GABRP|2569:GABRR1|200959:GABRR3|2570:GABRR2|55879:GABRQ|1134:CHRNA1|1135:CHRNA2|1136:CHRNA3|1137:CHRNA4|1138:CHRNA5|8973:CHRNA6|1139:CHRNA7|55584:CHRNA9|57053:CHRNA10|1140:CHRNB1|1141:CHRNB2|1142:CHRNB3|1143:CHRNB4|1144:CHRND|1145:CHRNE|1146:CHRNG|5023:P2RX1|22953:P2RX2|5024:P2RX3|5025:P2RX4|5026:P2RX5|5027:P2RX7|9127:P2RX6|1081:CGA|3972:LHB|2890:GRIA1|2891:GRIA2|2892:GRIA3|2893:GRIA4|2897:GRIK1|2898:GRIK2|2899:GRIK3|2900:GRIK4|2901:GRIK5|2894:GRID1|2895:GRID2|2741:GLRA1|2742:GLRA2|8001:GLRA3|2743:GLRB|7442:TRPV1|706:TSPO|2908:NR3C1|1442:CSH1|2689:GH2|2688:GH1|2690:GHR|7067:THRA|7068:THRB|3952:LEP|3953:LEPR|5617:PRL|5618:PRLR	Syndromic X-linked mental retardation with epilepsy or seizures|46,XY disorders of sex development (Disorders in androgen synthesis or action)|46,XY disorders of sex development (Other)|Premature ovarian failure|Woolly hair|Primary failure of tooth eruption|Waardenburg syndrome (WS)|Nonsyndromic autosomal recessive mental retardation (NS-ARMR)|Hyperekplexia|Congenital myasthenic syndrome|Febrile seizures|Congenital stationary night blindness (CSNB)|Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE)|Idiopathic generalied epilepsies (IGEs)|ABCD syndrome|Hirschsprung disease (HD)|Precocious puberty|Multiple pterygium syndrome|Ovarian hyperstimulation syndrome (OHSS)|Plasminogen deficiency	Glycine (JP16/USP)|Gamma-Aminobutyric acid (JAN)|Levodopa (JP16/USP/INN)|Noradrenaline (JP16)|Dinoprostone (JAN/USP/INN)|Dinoprost (JP16/USAN/INN)|Hydrocortisone (JP16/USP/INN)|Oxytocin (JP16/USP/INN)|Thrombin (JP16/USP/INN)|Adrenaline (JP16)|Vasopressin (JP16/USP)|Epoprostenol (USAN/INN)|Atropine (USP)|Glucagon (JAN/USP/INN)|Ephedrine (USP)|Haloperidol (JP16/USP/INN)|Scopolamine (INN)|Corticotropin (USP/INN)|Hyoscyamine (USP)|Hydrocortisone acetate (JP16/USP)|Protirelin (JP16/USAN/INN)|Alprostadil (JP16/USP/INN)|Argatroban hydrate (JP16)|Codeine (USP)|Alprazolam (JP16/USP/INN)|Aminophylline (USP/INN)|Methyloctatropine bromide (JAN)|Astemizole (JAN/USP/INN)|Atenolol (JP16/USP/INN)|Baclofen (JP16/USP/INN)|Betamethasone (JP16/USP/INN)|Budesonide (JAN/USAN/INN)|Calcitonin (salmon) (JP16)|Capsaicin (JAN/USP)|Carvedilol (JAN/USAN/INN)|Chlordiazepoxide (JP16/USP/INN)|Chlorpromazine (USP/INN)|Cisapride (USAN/INN)|Clonazepam (JP16/USP/INN)|Clonidine (JAN/USP/INN)|Clozapine (JAN/USP/INN)|Cosyntropin (USAN)|Desmopressin (INN)|Dexamethasone (JP16/USP/INN)|Diazepam (JP16/USP/INN)|Cimetidine (JP16/USP/INN)|Diphenhydramine (JP16/INN)|Dronabinol (USP/INN)|Droperidol (JP16/USP/INN)|Estazolam (JP16/USAN/INN)|Famotidine (JP16/USP/INN)|Fentanyl (JAN/USAN/INN)|Flunisolide (JAN/USP)|Fluocinonide (JP16/USP/INN)|Fludroxycortide (JAN/INN)|Flurazepam (JP16/INN)|Furosemide (JP16/USP/INN)|Latanoprost (JAN/USAN/INN)|Losartan potassium (JP16/USAN)|Liotrix (USP)|Loratadine (JAN/USAN/INN)|Lorazepam (JP16/USP/INN)|Lypressin (USP/INN)|Temazepam (USP/INN)|Theophylline (JP16)|Thioridazine (USP/INN)|Tiotixene (JAN)|Meprobamate (JAN/USP/INN)|Timolol (USAN)|Triamcinolone (JP16/USP/INN)|Triazolam (JAN/USP/INN)|Triflupromazine (USP/INN)|Tropicamide (JP16/USP/INN)|Valsartan (JAN/USAN/INN)|Levomepromazine (USAN/INN)|Methyldopa hydrate (JP16)|Methylprednisolone (JP16/USP/INN)|Zafirlukast (JAN/USAN/INN)|Zolmitriptan (JAN/USAN/INN)|Misoprostol (JAN/USAN/INN)|Ranitidine (USAN/INN)|Risperidone (JP16/USAN/INN)|Secobarbital (USP/INN)|Nadolol (JP16/USP/INN)|Nizatidine (JP16/USP/INN)|Octreotide (USAN/INN)|Sumatriptan (JAN/USP/INN)|Olanzapine (JAN/USAN/INN)|Quazepam (JAN/USP/INN)|Quetiapine fumarate (JAN/USAN)|Oxybutynin (USAN/INN)|Prazepam (JP16/USAN/INN)|Prednisolone (JP16/USP/INN)|Prednisone (USP)|Prochlorperazine maleate (JP16/USP)|Promethazine hydrochloride (JP16/USP)|Propantheline bromide (JP16/USP/INN)|Propoxyphene hydrochloride (USP)|Propranolol hydrochloride (JP16/USP)|Pseudoephedrine hydrochloride (USP)|Pancuronium bromide (JP16/USAN/INN)|Prochlorperazine (JAN/USP/INN)|Promethazine (JAN/INN)|Pentazocine (JP16/USP/INN)|Pentobarbital (USP/INN)|Pentobarbital sodium (JAN/USP)|Pergolide mesilate (JAN)|Perphenazine (JP16/USP/INN)|Phenobarbital (JP16/USP/INN)|Phenoxybenzamine hydrochloride (USP)|Phentolamine mesilate (JAN/INN)|Phenylephrine hydrochloride (JP16/USP)|Pindolol (JP16/USP/INN)|Dexmedetomidine (USAN/INN)|Dimenhydrinate (JP16/USP/INN)|Terfenadine (JAN/USAN/INN)|Candesartan (USAN/INN)|Irbesartan (JAN/USAN/INN)|Carbachol (JAN/USP/INN)|Pilocarpine (JAN/USP)|Anhydrous caffeine (JP16)|Montelukast sodium (JAN/USAN)|Nitrazepam (JP16/USAN/INN)|Glutethimide (JAN/INN)|Topiramate (JAN/USAN/INN)|Glycopyrronium bromide (JAN/INN)|Propofol (JAN/USAN/INN)|Midazolam (JAN/USP/INN)|Amobarbital (JP16/INN)|Methaqualone (JAN/USAN/INN)|Pramipexole hydrochloride hydrate (JAN)|Pimozide (JP16/USP/INN)|Sertindole (USAN/INN)|Mirtazapine (JAN/USAN/INN)|Goserelin acetate (JAN)|Acebutolol hydrochloride (JP16/USP)|Betaxolol hydrochloride (JP16/USP)|Carteolol hydrochloride (JP16/USP)|Labetalol hydrochloride (JP16/USP)|Metoprolol tartrate (JP16/USP)|Penbutolol sulfate (JP16/USP)|Timolol maleate (JP16/USP)|Clonidine hydrochloride (JP16/USP)|Guanabenz acetate (JP16/USP)|Guanfacine hydrochloride (JAN/USP)|Guanadrel sulfate (USP)|Doxazosin mesilate (JP16)|Prazosin hydrochloride (JP16/USP)|Terazosin hydrochloride hydrate (JAN)|Mecamylamine hydrochloride (USP)|Fenoldopam mesylate (USP)|Candesartan cilexetil (JP16/USAN)|Telmisartan (JAN/USAN/INN)|Dobutamine hydrochloride (JP16/USP)|Dopamine hydrochloride (JP16/USP)|Bisoprolol fumarate (JP16/USP)|Metoprolol succinate (USP)|Amiodarone hydrochloride (JP16/USAN)|Esmolol hydrochloride (JAN/USAN)|Tolterodine (USAN/INN)|Azelastine hydrochloride (JP16/USAN)|Cevimeline hydrochloride hydrate (JAN)|Azatadine maleate (USP)|Brompheniramine maleate (USAN)|Cetirizine hydrochloride (JP16/USAN)|Chlorpheniramine maleate (JP16/USP)|Clemastine fumarate (JP16/USP)|d-Chlorpheniramine maleate (JP16)|Diphenhydramine hydrochloride (JP16/USP)|Fexofenadine hydrochloride (JP16/USAN)|Hydroxyzine hydrochloride (JP16/USP)|Ranitidine hydrochloride (JP16/USP)|Naratriptan hydrochloride (JAN/USAN)|Rizatriptan benzoate (JAN/USAN)|Sumatriptan succinate (JAN/USAN)|Ergotamine tartrate (JP16/USP)|Methylergometrine maleate (JP16)|Methysergide maleate (USP)|Carboprost tromethamine (USP)|Salbutamol sulfate (JP16)|Bitolterol mesilate (JAN)|Orciprenaline sulfate (JP16)|Pirbuterol acetate (USAN)|Salmeterol xinafoate (JAN/USAN)|Terbutaline sulfate (JP16/USP)|Beclometasone dipropionate (JP16)|Mometasone furoate (JAN/USP)|Chlordiazepoxide hydrochloride (JAN/USP)|Clorazepate dipotassium (JP16/USP)|Flurazepam hydrochloride (USP)|Midazolam hydrochloride (USAN)|Mephobarbital (JAN/USP)|Phenobarbital sodium (JAN/USP/INN)|Buspirone hydrochloride (USP)|Zolpidem tartrate (JP16/USAN)|Ketamine hydrochloride (JP16/USP)|Thiamylal sodium (JP16)|Thiopental sodium (JP16/USP/INN)|Hyoscine methobromide (INN)|Dicyclomine hydrochloride (JAN/USP)|Hyoscyamine sulfate (USP)|Mepenzolate bromide (JP16/INN)|Methanthelinium bromide (INN)|Oxybutynin hydrochloride (JAN)|Tridihexethyl chloride (BAN)|Metoclopramide (JP16/INN)|Naphazoline hydrochloride (JP16/USP)|Methylprednisolone sodium succinate (JAN/USP)|Tetrahydrozoline nitrate (JAN)|Atracurium besylate (USP)|Cisatracurium besylate (USAN)|Doxacurium chloride (USAN/INN)|Mivacurium chloride (USAN/INN)|Pipecuronium bromide (USAN/INN)|Rocuronium bromide (JAN/USAN/INN)|Succinylcholine chloride (USP)|Vecuronium bromide (JAN/USAN/INN)|Orphenadrine citrate (USP)|Tizanidine hydrochloride (JP16/USAN)|Amantadine hydrochloride (JP16/USP)|Benztropine mesilate (JAN)|Biperiden (JAN/USP/INN)|Bromocriptine mesilate (JP16)|Procyclidine hydrochloride (USP)|Ropinirole hydrochloride (JAN/USAN)|Trihexyphenidyl hydrochloride (JP16/USP)|Chlorpromazine hydrochloride (JP16/USP)|Fluphenazine hydrochloride (JAN/USP)|Fluphenazine enanthate (JP16/USP)|Fluphenazine decanoate (JAN/USP)|Loxapine succinate (USP)|Molindone hydrochloride (USP)|Promazine hydrochloride (USP)|Thioridazine hydrochloride (JP16/USP)|Trifluoperazine hydrochloride (JAN/USP)|Triflupromazine hydrochloride (JAN/USP)|Nefazodone hydrochloride (USAN)|Trazodone hydrochloride (JAN/USP)|Alfentanil hydrochloride (USP)|Buprenorphine hydrochloride (JP16/USP)|Butorphanol tartrate (JAN/USP)|Dezocine (USAN)|Hydromorphone hydrochloride (USP)|Levomethadyl acetate hydrochloride (USAN)|Levorphanol tartrate (USP)|Morphine sulfate hydrate (JAN)|Nalbuphine hydrochloride (USAN)|Oxymorphone hydrochloride (USP)|Sufentanil citrate (USP)|Oxycodone hydrochloride (USP)|Dextromethorphan hydrobromide hydrate (JP16)|Betamethasone sodium phosphate (JP16/USP)|Cortisone acetate (JP16/USP)|Dexamethasone sodium phosphate (JAN/USP)|Hydrocortisone cypionate|Hydrocortisone sodium phosphate (JP16/USP)|Hydrocortisone sodium succinate (JP16/USP)|Methylprednisolone acetate (JAN/USP)|Prednisolone acetate (JP16/USP/INN)|Prednisolone sodium phosphate (JP16/USP)|Prednisolone tebutate (JAN/USP)|Triamcinolone acetonide (JP16/USP)|Triamcinolone diacetate (JAN/USP)|Triamcinolone hexacetonide (USP/INN)|Fludrocortisone acetate (JP16/USP)|Cabergoline (JAN/USAN/INN)|Gonadorelin hydrochloride (USP)|Leuprorelin acetate (JAN)|Nafarelin acetate (JAN/USAN)|Epinephrine hydrochloride (JAN)|Tolazoline hydrochloride (JAN/USP)|Acetylcholine chloride (JP16/USP/INN)|Bethanechol chloride (JP16/USP)|Cyclopentolate hydrochloride (JP16/USP)|Hexocyclium metilsulfate (INN)|Homatropine hydrobromide (JP16/USP)|Isopropamide iodide (JAN/USP/INN)|Oxyphencyclimine hydrochloride (JAN)|Propiverine hydrochloride (JP16)|Apraclonidine hydrochloride (JAN/USP)|Levothyroxine sodium hydrate (JP16)|Liothyronine sodium (JP16/USAN)|Dried thyroid (JP16)|Dipivefrin hydrochloride (JAN/USP)|Metaraminol bitartrate (JAN/USP)|Methoxamine hydrochloride (JAN)|Naphazoline nitrate (JP16)|Oxymetazoline hydrochloride (JAN/USP)|Tetrahydrozoline hydrochloride (JAN/USP)|Tamsulosin hydrochloride (JP16/USAN)|Levobunolol hydrochloride (JAN/USP)|Sotalol hydrochloride (JAN/USP)|Flupentixol (INN)|Spiperone (JAN/USAN)|Hexobarbital (JAN/INN)|Atropine methonitrate (JAN/INN)|Hydroxyzine pamoate (JP16/USP)|Bromperidol (JAN/USAN/INN)|Trospium chloride (JAN/USAN/INN)|Moperone hydrochloride (JAN)|Profenamine hydrochloride (JAN)|Seratrodast (JAN/USAN/INN)|Ramatroban (JAN/INN)|Lafutidine (JAN/INN)|Isothipendyl hydrochloride (JAN)|Tolterodine tartrate (JAN/USAN)|Ergometrine maleate (JP16)|Aripiprazole (JAN/USAN/INN)|Piperidolate hydrochloride (JAN)|Diphenylpyraline hydrochloride (JAN)|Pheniramine maleate (JAN/USP)|Carpronium chloride (JAN/INN)|Blonanserin (JAN/INN)|Remifentanil hydrochloride (JAN/USAN)|Alprenolol hydrochloride (JP16/USAN)|Pimilprost (JAN/INN)|Olopatadine hydrochloride (JAN/USAN)|Osutidine (JAN/INN)|Tiemonium iodide (JAN/INN)|Olmesartan medoxomil (JAN/USAN)|Dexmedetomidine hydrochloride (JAN/USAN)|Tolvaptan (JAN/USAN/INN)|Sulpiride (JP16/USAN/INN)|Bosentan hydrate (JAN)|Paramethasone acetate (JAN/USP)|Flunitrazepam (JP16/USAN/INN)|Piroheptine hydrochloride (JAN)|Conivaptan hydrochloride (JAN/USAN)|Prednisolone sodium succinate (JP16/USP)|Promethazine teoclate (JAN/INN)|Bromazepam (JP16/USAN/INN)|Clobazam (JAN/USAN/INN)|Tofisopam (JP16/INN)|Ritodrine hydrochloride (JP16/USP)|Cloxazolam (JP16/INN)|Solifenacin succinate (JAN/USAN/INN)|Clobetasol propionate (JP16/USP)|Clobetasone butyrate (JAN/USAN)|Oxazolam (JP16/INN)|Flutoprazepam (JP16/INN)|Flutazolam (JAN/INN)|Medazepam (JP16/INN)|Ethyl loflazepate (JAN/INN)|Cinnarizine (JAN/USAN/INN)|Pirenzepine hydrochloride (USAN)|Midodrine hydrochloride (JAN/USAN)|Secobarbital sodium (JAN/USP)|Methylbenactyzium bromide (JP16/INN)|Mexazolam (JAN/INN)|Meclizine hydrochloride (JAN/USP)|Zotepine (JAN/INN)|Mequitazine (JP16/INN)|Diflorasone diacetate (JAN/USP)|Clotiazepam (JP16/INN)|Ketotifen fumarate (JP16/USAN)|Urapidil (JP16/INN)|Carbinoxamine maleate (JAN/USP)|Epoprostenol sodium (JAN/USAN)|Naloxone hydrochloride (JP16/USP)|Dimetindene maleate (JAN)|Tramazoline hydrochloride (JAN/USAN)|Terguride (JAN/INN)|Pirbuterol hydrochloride (JAN/USAN)|Dinoprost tromethamine (JAN/USP)|Fludiazepam (JP16/INN)|Tramadol hydrochloride (JAN/USAN)|Betamethasone valerate (JP16/USP)|Mianserin hydrochloride (JAN/USAN)|Etomidoline (JAN/INN)|Clenbuterol hydrochloride (JAN/USP)|Tulobuterol hydrochloride (JP16)|Fluorometholone (JP16/USP/INN)|Bevantolol hydrochloride (JAN/USAN)|Zopiclone (JAN/INN)|Formoterol fumarate (USAN)|Prifinium bromide (JAN/INN)|Pethidine hydrochloride (JP16)|Ibudilast (JP16/INN)|Ephedrine hydrochloride (JP16/USP)|Amcinonide (JAN/USP/INN)|dl-Isoprenaline hydrochloride (JAN)|Fentanyl citrate (JP16/USP)|Betamethasone acetate (JAN/USP)|Norfenefrine hydrochloride (JAN)|Flurazepam hydrochloride (JP16)|Fenoterol hydrobromide (JAN)|Perlapine (JAN/USAN/INN)|Hydrocortisone succinate (JP16)|Bunitrolol hydrochloride (JAN)|Ifenprodil tartrate (JP16)|Thioproperazine mesilate (JAN)|Trifluoperazine maleate (JAN)|Scopolamine butylbromide (JP16)|Isopropyl unoprostone (JAN)|Caffeine hydrate (JP16)|Bupranolol hydrochloride (JP16)|Homochlorcyclizine hydrochloride (JP16)|Lisuride maleate (JAN)|Diponium bromide (JAN/INN)|Flumetasone pivalate (JAN/BAN)|Roxatidine acetate hydrochloride (JP16/USAN)|Nemonapride (JAN/INN)|Amosulalol hydrochloride (JP16)|Esatenolol (JAN/INN)|Ebastine (JP16/USAN/INN)|Dihydrocodeine phosphate (JP16)|Pipamperone hydrochloride (JAN)|Propericiazine (JAN)|Butropium bromide (JP16/INN)|Trimebutine maleate (JP16)|Bufetolol hydrochloride (JP16)|Talipexole hydrochloride (JAN)|Dexamethasone metasulfobenzoate sodium (JAN)|Befunolol hydrochloride (JAN)|Etizolam (JP16/INN)|Levomepromazine hydrochloride (JAN/USAN)|Pipethanate hydrochloride (JAN)|Tiapride hydrochloride (JP16)|Valethamate bromide (JAN)|Nylidrin hydrochloride (JAN)|Mosapramine hydrochloride (JAN)|Beraprost sodium (JP16/USAN)|Rilmazafone hydrochloride hydrate (JAN)|Moxisylyte hydrochloride (JAN)|Etilefrine hydrochloride (JP16)|Mabuterol hydrochloride (JAN)|Nimetazepam (JAN/INN)|Diphenylpiperidinomethyldioxolan iodide (JAN)|Dexamethasone palmitate (JAN)|Hydrocortisone butyrate (JP16/USP)|Sarpogrelate hydrochloride (JP16)|Diphenylpyraline teoclate (JAN)|Dexamethasone propionate (JAN)|Methoxyphenamine hydrochloride (JAN)|Betamethasone dipropionate (JP16/USP)|Hyoscyamine methylbromide (JAN)|Bepotastine besilate (JAN)|Lormetazepam (JAN/USAN/INN)|Naftopidil (JAN/INN)|Cetrorelix acetate (JAN/USAN)|Loteprednol etabonate (JAN/USAN)|Nipradilol (JAN/INN)|Alfuzosin hydrochloride (JAN/USAN)|Dalcotidine (JAN/INN)|Darifenacin hydrobromide (JAN/USAN)|Ciclesonide (JAN/USAN/INN)|Fluticasone propionate (JAN/USAN)|Epinastine hydrochloride (JAN)|Levocabastine hydrochloride (JAN/USAN)|Barbital (JP16/INN)|Celiprolol hydrochloride (JAN/USAN)|Clebopride malate (JP16)|Brotizolam (JAN/USAN/INN)|Domperidone (JP16/USAN/INN)|Isoxsuprine hydrochloride (JP16/USP)|Haloxazolam (JP16/INN)|Proxyphylline (JAN/INN)|Oxatomide (JAN/USAN/INN)|Triprolidine hydrochloride hydrate (JAN)|Bopindolol malonate (JAN)|Oxprenolol hydrochloride (JP16/USP)|Oxapium iodide (JP16/INN)|Proglumide (JP16/USAN/INN)|Alclometasone dipropionate (JAN/USP)|Fluocinolone acetonide (JP16/USP/INN)|Arotinolol hydrochloride (JP16)|Buserelin acetate (JAN/USAN)|Landiolol hydrochloride (JAN)|Mozavaptane hydrochloride (JAN)|Panazepide (JAN)|Pibutidine hydrochloride (JAN)|Ornoprostil (JAN/INN)|Metixene hydrochloride (JAN)|Tiquizium bromide (JAN/INN)|Eptazocine hydrobromide (JAN)|Hydrocortisone butyrate propionate (JAN)|Bunazosin hydrochloride (JP16)|Enprostil (JAN/USAN/INN)|Haloperidol decanoate (JAN/USAN)|Dimetotiazine mesilate (JAN)|Taltirelin hydrate (JAN)|Tiotropium bromide hydrate (JAN)|Ziprasidone hydrochloride hydrate (JAN)|Oxitropium bromide (JAN/INN)|Dexamethasone valerate (JAN)|L-Methylephedrine hydrochloride (JAN)|Aclatonium napadisilate (JAN)|Travoprost (JAN/USAN/INN)|Silodosin (JAN/INN)|Eletriptan hydrobromide (JAN/USAN)|N-Methylscopolamine methylsulfate (JAN)|Trimetoquinol hydrochloride|Ximelagatran (JAN/USAN/INN)|Pipethanate ethobromide (JAN)|Tandospirone citrate (JAN/USAN)|Mosapride citrate hydrate (JP16)|Prednisolone farnesylate (JAN)|Apomorphine hydrochloride hydrate (JAN)|Protirelin tartrate hydrate (JP16)|Secretin (JAN/USAN/INN)|Prochlorperazine mesilate (JAN)|Betamethasone butyrate propionate (JAN)|Setiptiline maleate (JAN)|Timiperone (JAN)|Perphenazine maleate (JP16)|Clinprost (JAN/INN)|Isoprenaline sulfate (JAN)|Atropine sulfate (JP16/USP)|Homatropine methylbromide (USP)|Scopolamine hydrobromide hydrate (JP16)|Gemeprost (JAN/USAN/INN)|Brimonidine tartrate (JAN/USAN)|Metipranolol hydrochloride|Eprosartan mesylate (USAN)|Cyclizine lactate (BAN)|Tripelennamine hydrochloride (USP)|Cisapride (JAN)|Isoetharine hydrochloride (USP)|Naltrexone hydrochloride (USP)|Ziprasidone mesylate (USAN)|Codeine phosphate hydrate (JP16)|Methadone hydrochloride (USP)|Nalmefene hydrochloride|Tetracosactide acetate (JAN)|Indium In 111 pentetreotide (USP)|dl-Methylephedrine hydrochloride (JP16)|Pentazocine lactate (USP)|Histrelin acetate|Sermorelin acetate (USAN)|Glucagon hydrochloride|Albuterol (USP)|Phenindamine tartrate (USAN)|Epinephrine bitartrate (JAN/USP)|l-Isoprenaline hydrochloride (JP16)|Tulobuterol (JAN/INN)|Prednisolone succinate (JP16)|Fluphenazine maleate (JAN)|Dexamethasone acetate (JAN/USP)|Pilocarpine hydrochloride (JP16/USP)|Hexamethonium bromide (JAN/INN)|Ethylmorphine hydrochloride hydrate (JP16)|Tubocurarine chloride hydrate (JAN)|Sultopride hydrochloride (JAN)|Dihydroergotamine mesilate (JP16)|Ipratropium bromide hydrate (JP16)|Metoclopramide hydrochloride (JAN)|Pentazocine hydrochloride (JAN/USP)|Cyproheptadine hydrochloride (JP16/USP)|Desmopressin acetate hydrate (JAN)|Flupentixol dihydrochloride (JAN)|Levallorphan tartrate (JP16)|Alimemazine tartrate (JP16)|Biperiden hydrochloride (JP16/USP)|Biperiden lactate (JAN/USP)|Levomepromazine maleate (JP16/USAN)|Emedastine difumarate (JAN/USP)|Octreotide acetate (JAN)|Amobarbital sodium (JP16/USP)|Pentobarbital calcium (JP16)|Morphine hydrochloride hydrate (JP16)|Suxamethonium chloride hydrate (JP16)|Levalbuterol hydrochloride (USAN)|Betamethasone benzoate (USP)|Clocortolone pivalate (USP)|Hydrocortisone valerate (USP)|Medrysone (USAN)|Gallamine triethiodide (USP)|Doxylamine succinate (USP)|Acebutolol (USAN/INN)|Loxapine (USAN/INN)|Bisoprolol (JAN/USAN/INN)|Carboprost (USAN/INN)|Dipivefrin (USAN)|Methysergide (USAN/INN)|Metoprolol (USAN/INN)|Ritodrine (USAN/INN)|Ketanserin (USAN/INN)|Histrelin (USAN/INN)|Clocapramine hydrochloride hydrate (JP16)|Perospirone hydrochloride hydrate (JAN)|Metipranolol (USAN/INN)|Verlukast (USAN/INN)|Levonordefrin (USP)|Primidolol (USAN/INN)|Hexoprenaline sulfate (USAN)|Procaterol hydrochloride (USAN)|Selfotel (USAN/INN)|Flutropium bromide (JAN)|Diphenhydramine salicylate (JAN)|Timepidium bromide hydrate (JP16)|Kainic acid hydrate (JP16)|Flesinoxan (INN)|Eptapirone (INN)|Flibanserin (USAN/INN)|Agomelatine (INN)|Montirelin (INN)|Dexamethasone acefurate (USAN/INN)|Dexamethasone beloxil (USAN)|Orphenadrine hydrochloride|Methoxypromazine maleate|Prochlorperazine edisylate (USP)|Thiothixene hydrochloride (USP)|Clopenthixol (USAN)|Denopamine (JAN/INN)|Pagoclone (USAN/INN)|Ocinaplon (USAN/INN)|Pipamperone (USAN/INN)|Moperone (INN)|Eszopiclone (JAN/USAN/INN)|Trifluperidol (USAN/INN)|Bromperidol decanoate (USAN)|Butaclamol hydrochloride (USAN)|Iloperidone (USAN/INN)|Mazapertine succinate (USAN)|Oxiperomide (USAN/INN)|Piquindone hydrochloride (USAN)|Remoxipride (USAN)|Remoxipride hydrochloride (USAN)|Tiospirone hydrochloride (USAN)|Ramelteon (JAN/USAN/INN)|Somatropin (genetical recombination) (JAN)|Human menopausal gonadotrophin (JP16)|Devazepide (USAN/INN)|Talampanel (INN)|Talibegron hydrochloride (USAN)|Alprostadil alfadex (JP16)|Tarazepide (INN)|Rosaprostol (INN)|Beraprost (USAN)|Iloprost (USAN/INN)|Limaprost (INN)|Sulprostone (USAN/INN)|Tegaserod maleate (USAN)|Pranlukast hydrate (JAN)|Abarelix (USAN/INN)|Ablukast (USAN/INN)|Ablukast sodium (USAN)|Aceclidine (USAN/INN)|Acrivastine (USAN/INN)|Adatanserin hydrochloride (USAN)|Adrogolide hydrochloride (USAN)|Alemcinal (USAN/INN)|Almotriptan (USAN)|Almotriptan malate (USAN)|Alprenoxime hydrochloride (USAN)|Altanserin tartrate (USAN)|Altinicline maleate (USAN)|Cinalukast (USAN/INN)|Pobilukast edamine (USAN)|Ritolukast (USAN/INN)|Tomelukast (USAN/INN)|Limaprost alfadex (JP16)|Alvameline maleate (USAN)|Alvimopan (USAN)|Amesergide (USAN/INN)|Amiodarone (USAN/INN)|Antazoline phosphate (USP)|Apaxifylline (USAN/INN)|Aprepitant (JAN/USAN/INN)|Aptazapine maleate (USAN)|Aptiganel hydrochloride (USAN)|Arbutamine hydrochloride (USAN)|Arformoterol tartrate (USAN)|Argipressin tannate (USAN)|Asenapine maleate (USAN)|Atipamezole (USAN/INN)|Atosiban (USAN/INN)|Atrasentan hydrochloride (USAN)|Atropine oxide hydrochloride (USAN)|Avitriptan fumarate (USAN)|Bamifylline hydrochloride (USAN)|Benzetimide hydrochloride (USAN)|Besonprodil (USAN)|Binodenoson (USAN/INN)|Binospirone mesylate (USAN)|Bretazenil (USAN/INN)|Brifentanil hydrochloride (USAN)|Bromocriptine (USAN/INN)|Bucindolol hydrochloride (USAN)|Bunolol hydrochloride (USAN)|Butaprost (USAN/INN)|Butopamine (USAN/INN)|Butorphanol (USAN/INN)|Butoxamine hydrochloride (USAN)|Apadenoson (USAN)|Aplindore fumarate (USAN)|Atilmotin (USAN/INN)|Befetupitant (USAN/INN)|Mazaticol hydrochloride hydrate (JAN)|Gonadorelin diacetate (JP16)|Dinoprostone betadex (JAN)|Chlorpromazine hibenzate (JAN)|Profenamine hibenzate (JAN)|Diphenhydramine tannate (JP16)|Elcatonin (JP16/INN)|Promethazine methylenedisalicylate (JAN)|Prednisolone valerate acetate (JAN)|Mometasone furoate hydrate (JAN)|Teriparatide acetate (JAN)|Diphenhydramine laurylsulfate (JAN)|Carboprost methyl (USAN)|Carbuterol hydrochloride (USAN)|Carfentanil citrate (USAN)|Carvedilol phosphate hydrate (JAN)|Cetamolol hydrochloride (USAN)|Chlorpheniramine polistirex (USAN)|Choriogonadotropin alfa (USAN/INN)|Cicloprolol hydrochloride (USAN)|Ciladopa hydrochloride (USAN)|Cimaterol (USAN/INN)|Cimetidine hydrochloride (USP)|Cinanserin hydrochloride (USAN)|Clebopride (USAN)|Clemastine (USAN)|Clocortolone acetate (USAN)|Zuclopenthixol (INN)|Cloprednol (USAN/INN)|Clorazepate monopotassium (USAN)|Codeine sulfate (USP)|Colterol mesylate (USAN)|Corticorelin acetate (USAN)|Corticorelin ovine triflutate (USAN)|Corticotropin zinc hydroxide (USP)|Cortivazol (USAN)|Cortodoxone (USAN)|Cyclazocine (USAN/INN)|Cyclizine (INN)|Cyclizine hydrochloride (USP)|Daltroban (USAN/INN)|Dapiprazole hydrochloride (USAN)|Darifenacin (USAN/INN)|Deflazacort (USAN/INN)|Delequamine hydrochloride (USAN)|Deltibant (USAN/INN)|Delucemine hydrochloride (USAN)|Desirudin (USAN/INN)|Desloratadine (USAN/INN)|Desonide (USAN/INN)|Desoximetasone (USP/INN)|Detomidine hydrochloride (USAN)|Dexbrompheniramine maleate (USAN)|Dexetimide (USAN/INN)|Dexfenfluramine hydrochloride (USAN)|Efegatran sulfate (USAN)|Napsagatran (USAN)|Dexpropranolol hydrochloride (USAN)|Dextofisopam (USAN/INN)|Dextromethorphan polistirex (USAN)|Dextrorphan hydrochloride (USAN)|Diacetolol hydrochloride (USAN)|Oxycodone terephthalate (USP)|Atropine methylbromide (JAN)|Dihydrocodeine bitartrate (USP)|Diphenhydramine citrate (USP)|Dizocilpine maleate (USAN)|Dobutamine (USP/INN)|Dobutamine lactobionate (USAN)|Dobutamine tartrate (USP)|Donetidine (USAN)|Dopexamine (USAN/INN)|Corticorelin (human) (JAN)|Ecopipam hydrochloride (USAN)|Edonentan (USAN)|Eglumetad (USAN)|Elzasonan citrate (USAN)|Elzasonan hydrochloride (USAN)|Ephedrine sulfate (USP)|Chlorpromazine phenolphthalinate (JAN)|Perphenazine fendizoate (JAN)|Eprosartan (USAN/INN)|Esoxybutynin chloride (USAN)|Ethybenztropine (USAN)|Etintidine hydrochloride (USAN)|Eucatropine hydrochloride (USP XXXII)|Exenatide (JAN/USAN/INN)|Ezlopitant (USAN/INN)|Fadolmidine hydrochloride (USAN)|Saralasin acetate (USAN)|Fenfluramine hydrochloride (USAN)|Fenobam (USAN)|Fenoterol (USAN/INN)|Fiduxosin hydrochloride (USAN)|Fingolimod hydrochloride (JAN/USAN)|Flestolol sulfate (USAN)|Flumethasone (USAN)|Flunisolide acetate (USAN)|Fluocortin butyl (USAN)|Fluocortolone (USAN/INN)|Fluocortolone caproate (USAN)|Fluorometholone acetate (USAN)|Fluparoxan hydrochloride (USAN)|Flupirtine maleate (USAN)|Fluprednisolone (USAN/INN)|Fluprednisolone valerate (USAN)|Forasartan (USAN/INN)|Fospropofol disodium (USAN)|Frovatriptan succinate (USAN)|Gaboxadol (USAN/INN)|Ganaxolone (USAN/INN)|Ganirelix acetate (JAN/USAN)|Gantacurium chloride (USAN/INN)|Gavestinel (USAN/INN)|Gepirone hydrochloride (USAN)|Gonadorelin acetate (USAN)|Guanabenz (USAN/INN)|Goserelin (USAN/INN)|Halobetasol propionate (USAN)|Follitropin alfa (genetical recombination) (JAN)|Follitropin beta (genetical recombination) (JAN)|Hydrocodone polistirex (USAN)|Hydrocortisone hemisuccinate (USP)|Hyoscyamine hydrobromide (USP)|Ibopamine (USAN/INN)|Icatibant acetate (USAN)|Icotidine (USAN)|Idremcinal (USAN/INN)|Ifetroban (USAN/INN)|Ifetroban sodium (USAN)|Imiloxan hydrochloride (USAN)|Impromidine hydrochloride (USAN)|Indoramin (USAN/INN)|Indoramin hydrochloride (USAN)|Indorenate hydrochloride (USAN)|Ipsapirone hydrochloride (USAN)|Isoetharine (USP)|Isoetharine mesylate (USP)|Istradefylline (JAN/USAN/INN)|Iturelix (USAN/INN)|Ketazocine (USAN/INN)|Lanreotide acetate (JAN/USAN)|Lavoltidine succinate (USAN)|Lecozotan hydrochloride (USAN)|Lergotrile (USAN/INN)|Lergotrile mesylate (USAN)|Levalbuterol tartrate (USAN)|Levdobutamine lactobionate (USAN)|Levobetaxolol hydrochloride (USAN)|Levomethadyl acetate (USAN)|Levonantradol hydrochloride (USAN)|Levotofisopam (USAN/INN)|Lexipafant (USAN/INN)|Licostinel (USAN/INN)|Lixivaptan (USAN/INN)|Lofentanil oxalate (USAN)|Lubazodone hydrochloride (USAN)|Lupitidine hydrochloride (USAN)|Lurasidone hydrochloride (JAN/USAN)|Lutropin alfa (USAN/INN)|Maropitant citrate (USAN)|Medazepam hydrochloride (USAN)|Medetomidine hydrochloride (USAN)|Medroxalol (USAN/INN)|Medroxalol hydrochloride (USAN)|Memantine hydrochloride (JAN/USAN)|Meptazinol hydrochloride (USAN)|Metaproterenol polistirex (USAN)|Perphenazine hydrochloride|Methacholine chloride (USAN/INN)|Methadyl acetate (USAN)|Methylprednisolone succinate (JP16)|Methylprednisolone sodium phosphate (USAN)|Methylprednisolone suleptanate (USAN/INN)|Metiamide (USAN/INN)|Metkephamid acetate (USAN)|Metoclopramide hydrochloride (USAN)|Metopimazine (USAN/INN)|Metoprolol fumarate (USP)|Metreleptin (USAN/INN)|Metrenperone (USAN/INN)|Midazolam maleate (USAN)|Milameline hydrochloride (USAN)|Trimetoquinol hydrochloride hydrate (JP16)|Mirfentanil hydrochloride (USAN)|Mitemcinal fumarate (USAN)|Nabilone (USAN/INN)|Nalmefene (USAN/INN)|Naltrexone (USAN/INN)|Nebivolol (USAN/INN)|Neramexane mesylate (USAN)|Norepinephrine bitartrate (USP)|Ocfentanil hydrochloride (USAN)|Octreotide pamoate (USAN)|Olmesartan (USAN/INN)|Serum gonadotrophin (JP16)|Pirenzepine hydrochloride hydrate (JP16)|Formoterol fumarate hydrate (JP16)|Oxmetidine hydrochloride (USAN)|Oxmetidine mesylate (USAN)|Oxycodone (USAN/INN)|Paliperidone (JAN/USAN/INN)|Paliperidone palmitate (JAN/USAN)|Pamatolol sulfate (USAN)|Parathyroid hormone (human) (USAN)|Procaterol hydrochloride hydrate (JP16)|Pegvisomant (genetical recombination) (JAN)|Pelanserin hydrochloride (USAN)|Aminophylline hydrate (JP16)|Perzinfotel (USAN/INN)|Phencyclidine hydrochloride (USAN)|Oxycodone hydrochloride hydrate (JP16)|Piboserod hydrochloride (USAN)|Picumeterol fumarate (USAN)|Pilocarpine nitrate (USP)|Pizotyline (USAN)|Pramipexole (USAN/INN)|Practolol (USAN)|Prednicarbate (USP/INN)|Prenalterol hydrochloride (USAN)|Propoxyphene napsylate (USAN)|Pseudoephedrine polistirex (USAN)|Pseudoephedrine sulfate (USP)|Quinelorane hydrochloride (USAN)|Quinpirole hydrochloride (USAN)|Raclopride C11 (USP)|Ranitidine bismuth citrate (USAN)|Rapacuronium bromide (USAN/INN)|Regadenoson (USAN/INN)|Remacemide hydrochloride (USAN)|Reproterol hydrochloride (USAN)|Ridogrel (USAN/INN)|Rimexolone (USP/INN)|Rimiterol hydrobromide (USAN)|Rimonabant (JAN/USAN/INN)|Rioprostil (USAN/INN)|Ritanserin (USAN/INN)|Rizatriptan sulfate (USAN)|Rotigotine (JAN/USAN/INN)|Salmeterol (USAN/INN)|Sarizotan hydrochloride (USAN)|Selodenoson (USAN/INN)|Sibenadet hydrochloride (USAN)|Solabegron hydrochloride (USAN)|Somatrem (genetical recombination) (JAN)|Sonepiprazole mesylate (USAN)|Spiradoline mesylate (USAN)|Sufentanil (USAN/INN)|Sufotidine (USAN/INN)|Sulamserod hydrochloride (USAN)|Sulotroban (USAN/INN)|Talnetant hydrochloride (USAN)|Talsaclidine fumarate (USAN)|Tecadenoson (USAN/INN)|Tegaserod (USAN/INN)|Teriparatide (genetical recombination) (JAN)|Thiamylal|Thyrotropin alfa (genetical recombination) (JAN)|Tiotidine (USAN/INN)|Tixocortol pivalate (USAN)|Traxoprodil mesylate (USAN)|Trefentanil hydrochloride (USAN)|Treprostinil (JAN/USAN/INN)|Triamcinolone acetonide sodium phosphate (USAN)|Tripelennamine citrate|Triptorelin (USAN/INN)|Triptorelin pamoate (USAN)|Tropanserin hydrochloride (USAN)|Trimeperidine (INN)|Urofollitropin (USAN/INN)|Imidafenacin (JAN/INN)|Tafluprost (JAN/USAN/INN)|Vapiprost hydrochloride (JAN/USAN)|Vapreotide (USAN/INN)|Fluticasone furoate (JAN/USAN/INN)|Vofopitant dihydrochloride (USAN)|Xamoterol (USAN)|Xamoterol fumarate (USAN)|Xanomeline (USAN)|Xanomeline tartrate (USAN)|Zacopride hydrochloride (USAN)|Zaltidine hydrochloride (USAN)|Zucapsaicin (USAN/INN)|Enadoline hydrochloride (USAN)|Renzapride (INN)|Follitropin alfa/beta|Liraglutide (genetical recombination) (JAN)|Nalfurafine hydrochloride (JAN)|Chorionic gonadotrophin (JP16)|Purified human menopausal gonadotrophin (JAN)|Serum gonadotrophin for injection (JP16)|Thyroid (USP)|Octreotide acetate (USAN)|Corticotropin, repository (USP)|Teriparatide acetate (USAN)|Alcaftadine (USAN/INN)|Bifeprunox mesylate (USAN)|Casopitant mesylate (USAN)|Fosaprepitant meglumine (JAN)|Lorcaserin hydrochloride (USAN)|Methylnaltrexone bromide (USAN)|Nebivolol hydrochloride (USAN)|Olanzapine pamoate (USAN)|Pruvanserin (USAN/INN)|Pruvanserin hydrochloride (USAN)|Epanolol (USAN/INN)|Yohimbine hydrochloride (USP)|Terlipressin (USAN/INN)|Meprednisone (USP/INN)|Hydrocortisone aceponate (INN)|Lepirudin (INN)|Niperotidine (INN)|Dexamethasone cipecilate (JAN/INN)|Ambrisentan (JAN/INN)|Dabigatran etexilate methanesulfonate (JAN)|Cimetropium bromide (INN)|Alclometasone (INN)|Alfentanil (INN)|Alfuzosin (INN)|Alimemazine (INN)|Buprenorphine (JAN/INN)|Melagatran (INN)|Oxedrine (BAN)|Alprenolol (INN)|Mepindolol (INN)|Tertatolol (INN)|Cloranolol (INN)|Talinolol (INN)|Chlorphenoxamine (INN)|Fluprednidene (INN)|Methylprednisolone aceponate (INN)|Tiratricol (INN)|Quinagolide (INN/BAN)|Metergoline (INN)|Ornipressin (INN)|Demoxytocin (INN)|Carbetocin (INN/BAN)|Prednylidene (INN)|Buserelin (INN)|Esketamine (INN)|Diamorphine (BAN)|Levosulpiride (INN)|Choline alfoscerate (INN)|Bambuterol (INN)|Chlorphenamine (INN)|Levocetirizine (USAN/INN)|Pimethixene (INN)|Pentetrazol (INN)|Somatostatin (INN)|Amantadine (INN)|Amosulalol (INN)|Apomorphine (BAN)|Apraclonidine (INN)|Arformoterol (INN)|Arotinolol (INN)|Atosiban acetate|Atropine oxide (INN)|Azatadine (INN)|Azelastine (INN)|Bambuterol hydrocloride|Beclometasone (INN)|Benzatropine (INN)|Betaxolol (INN)|Bitolterol (INN)|Bopindolol (INN)|Bosentan (INN)|Brimonidine (INN)|Brompheniramine (INN)|Bunazosin (INN)|Buphenine (INN)|O-Acetyldihydrocodeine hydrochloride|Bupranolol (INN)|Buspirone (INN)|Carazolol (INN)|Carbinoxamine (INN)|Carfentanil (INN)|Carteolol (INN)|Celiprolol (INN)|Cetirizine (INN)|Cetrorelix (INN)|Cevimeline (INN)|Clazosentan sodium (JAN)|Chlorphenoxamine hydrochloride|Clenbuterol (INN)|Clobetasol (INN)|Clobetasone (INN)|Clocapramine (INN)|Clocortolone (INN)|Cinnarizine dihydrochloride|Codeine hydrochloride|Zibotentan (JAN/USAN/INN)|Conivaptan (INN)|Cortisone (INN)|Cyclopentolate (INN)|Cyproheptadine (INN)|Delorazepam (INN)|Dexamethasone 21-acetate|Dexamethasone isonicotinate|Dexamethasone sodium hemisulfate|Dexamethasone 21-tebutate|Dexamethasone 21-valerate|Dexamethasone phenylpropionate|Dexamethasone phosphate|Dexchlorpheniramine (INN)|Dexfenfluramine (INN)|Dextropropoxyphene (INN)|Diacetylmorphine hydrochloride|Dicycloverine (INN)|Diflorasone (INN)|Dihydrocodeine (INN)|Dihydrocodeine thiocyanate|Dihydroergotamine (INN)|Dihydroergotamine tartrate|Dimetindene (INN)|Dimetotiazine (INN)|Dioxopromethazine hydrochloride|Diphenylpyraline (INN)|Diprenorphine (INN)|Diprenorphine hydrochloride|Domperidone maleate|Dopamine (INN)|Doxazosin (INN)|Doxylamine (INN)|Eletriptan (INN)|Emedastine (INN)|Epinastine (INN)|Eptazocine (INN)|Ergometrine (INN)|Ergotamine (INN)|Esmolol (INN)|Ethylmorphine (BAN)|Etilefrine (INN)|Etorphine (INN)|Fentonium bromide (INN)|Fexofenadine (INN)|Fludrocortisone (INN)|Fluocortin (INN)|Fluocortolone 21-pivalate|Flupentixol decanoate|Fluphenazine (INN)|Fluprednidene acetate|Fluticasone (INN)|Formoterol (INN)|Frovatriptan (INN)|Sodium furosemide|Furosemide diolamine|Ganirelix (INN)|Velneperit (USAN/INN)|Gonadorelin (INN)|Guanfacine (INN)|Haloperidol lactate|Hexoprenaline (INN)|Histamine (DCF)|Homochlorcyclizine (INN)|Hydrocodone (INN)|Hydrocodone hydrochloride|Hydromorphone (INN)|Hydroxyzine (INN)|Ibopamine hydrochloride|Ifenprodil (INN)|Iloprost tromethamine|Azilsartan medoxomil (USAN)|Penbutolol (INN)|Isoprenaline (INN)|Isothipendyl (INN)|Isoxsuprine (INN)|Isoxsuprine lactate|Ketamine (INN)|Ketanserin tartrate|Ketotifen (INN)|Labetalol (INN)|Leuprorelin (INN)|Levobunolol (INN)|Levocetirizine hydrochloride (JAN/USAN)|Levomethadone (INN)|Levomethadone hydrochloride|Levorphanol (INN)|Levosalbutamol (INN)|Levothyroxine (BAN)|Liothyronine (INN)|Liothyronine hydrochloride|Lisuride (INN)|Losartan (INN)|Loteprednol (INN)|Mazaticol (INN)|Melatonin|Memantine (INN)|Meptazinol (INN)|Mepyramine (INN)|Mepyramine theophyllineacetate|Metaraminol (INN)|Methadone (BAN)|Methyldopa (INN)|Methylephedrine (BAN)|Methylergometrine (INN)|Mianserin (INN)|Midodrine (INN)|Mometasone (INN)|Montelukast (INN)|Morphine (BAN)|Morphine tartrate|Mosapramine (INN)|Mosapride (INN)|Moxisylyte (INN)|Nafarelin (INN)|Nalbuphine (INN)|Nalorphine (INN)|Nalorphine hydrochloride (USP)|Naloxone (INN)|Naphazoline (INN)|Naratriptan (INN)|Nefazodone (INN)|Nonivamide (INN)|Nordazepam (INN)|Norepinephrine hydrochoride|Norfenefrine (INN)|Olopatadine (INN)|Orciprenaline (INN)|Orphenadrine (INN)|Oxedrine tartrate|Oxedrine hydrochloride|Oxprenolol (INN)|Oxymetazoline (INN)|Oxymorphone (INN)|Oxyphencyclimine (INN)|Pergolide (INN)|Perphenazine decanoate|Perphenazine enantate|Pethidine (INN)|Phenindamine (INN)|Pheniramine (INN)|Phenobarbital diethylamine|Phenoxybenzamine (INN)|Phentolamine (INN)|Phenylephrine (INN)|Phenylephrine tartrate|Pilocarpine borate|Piperidolate (INN)|Pipethanate (INN)|Pirbuterol (INN)|Pirenzepine (INN)|Piroheptine (INN)|Pizotifen malate|Pranlukast (INN)|Prazosin (INN)|Prednisolone pivalate|Prednisolone sodium metazoate (USAN)|Prednisolone 21-(sodium tetrahydrophthalate)|Prednisolone steaglate (BAN)|Prednisone acetate|Procaterol (INN)|Procyclidine (INN)|Profenamine (INN)|Promethazine maleate|Propiverine (INN)|Propranolol (INN)|Pseudoephedrine (INN)|Quetiapine (INN)|Quinagolide hydrochloride (BAN)|Remifentanil (INN)|Reproterol (INN)|Rilmazafone (INN)|Rizatriptan (INN)|Ropinirole (USAN/INN)|Roxatidine (INN)|Roxatidine acetate (BAN)|Sarpogrelate (INN)|Sermorelin (INN)|Setiptiline (INN)|Solifenacin (INN)|Sotalol (INN)|Sultopride (INN)|Talipexole (INN)|Tamsulosin (INN)|Tandospirone (INN)|Terazosin (INN)|Terbutaline (INN)|Terlipressin acetate (JAN)|Tertatolol hydrochloride|Tetryzoline (INN)|Thioproperazine (INN)|Tiapride (INN)|Tiemonium methylsulfate|Timolol (INN)|Tixocortol (INN)|Tizanidine (INN)|Tolazoline (INN)|Tramadol (INN)|Tramazoline (INN)|Trazodone (INN)|Treprostinil monosodium salt|Tretoquinol (INN)|Degarelix acetate (USAN)|Trifluoperazine (INN)|Trifluperidol hydrochloride|Trihexyphenidyl (INN)|Trimebutine (INN)|Tripelennamine (INN)|Triprolidine (INN)|Triptorelin acetate|Unoprostone (INN)|Urapidil hydrochloride|Yohimbine (DCF)|Ziprasidone (INN)|Zolpidem (INN)|Zuclopenthixol acetate|Zuclopenthixol decanoate|Zuclopenthixol dihydrochloride|Promethazine hibenzate|Arbaclofen placarbil (USAN/INN)|Azilsartan (JAN/USAN/INN)|Corifollitropin alfa (INN/USAN)|Degarelix (INN/USAN)|Eglumegad (INN)|Ispronicline (INN/USAN)|Phenylephrine bitartrate (USP)|Prucalopride (USAN/INN)|Indacaterol (USAN/INN)|Indacaterol maleate (JAN/USAN)|Ibipinabant (USAN/INN)|Degarelix acetate (JAN)|Mirabegron (USAN/JAN)|Lixisenatide (JAN/INN)|Ritobegron ethyl hydrochloride (JAN)|Carpronium chloride hydrate (JAN)|Arbaclofen (USAN)|Norepinephrine hydrochloride (JAN)|Montirelin hydrate (JAN)|Cariprazine hydrochloride (JAN/USAN)|Pomaglumetad methionil (USAN/INN)|Almorexant (INN)|Ulimorelin (USAN/INN)|Ulimorelin hydrochloride (USAN)|Vipadenant (USAN/INN)|Selexipag (JAN/USAN/INN)|Cariprazine (USAN/INN)|Fingolimod (INN)|Eplivanserin (USAN/INN)|Olodaterol hydrochloride (JAN/USAN)|Dexmecamylamine (USAN)|Dexmecamylamine hydrochloride (USAN)	
hsa00670	One carbon pool by folate - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	1719:DHFR|25902:MTHFD1L|4522:MTHFD1|10797:MTHFD2|441024:MTHFD2L|6470:SHMT1|6472:SHMT2|2618:GART|471:ATIC|10841:FTCD|123263:MTFMT|275:AMT|4548:MTR|7298:TYMS|10840:ALDH1L1|160428:ALDH1L2|4524:MTHFR|10588:MTHFS|200895:DHFRL1	Homocystinuria|Spina bifida|AICA-ribosiduria|Dihydrofolate reductase (DHFR) deficiency	Methotrexate (JP16/USP/INN)|Fluorouracil (JP16/USP/INN)|Raltitrexed (JAN/USAN/INN)|Capecitabine (JAN/USAN/INN)|Tegafur (JP16/USAN/INN)|Doxifluridine (JP16/INN)|Carmofur (JP16/INN)|Methotrexate sodium|Tegafur - uracil mixt|Pemetrexed disodium (USAN)|Floxuridine (USP/INN)|Metesind glucuronate (USAN)|Pelitrexol (USAN/INN)|Pralatrexate (USAN/INN)|Trimetrexate (USAN/INN)|Trimetrexate glucuronate (USAN)|Pemetrexed sodium hydrate (JAN)|Pemetrexed (INN)|Fluorouracil sodium salt	
hsa00590	Arachidonic acid metabolism - Homo sapiens (human)	Metabolism; Lipid Metabolism	391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|151056:PLB1|239:ALOX12|242:ALOX12B|246:ALOX15|2882:GPX7|2880:GPX5|2877:GPX2|2878:GPX3|2876:GPX1|257202:GPX6|1562:CYP2C18|1559:CYP2C9|1557:CYP2C19|1558:CYP2C8|1573:CYP2J2|240:ALOX5|4056:LTC4S|2678:GGT1|2686:GGT7|2687:GGT5|124975:GGT6|4048:LTA4H|8529:CYP4F2|4051:CYP4F3|57834:CYP4F11|5742:PTGS1|5743:PTGS2|5730:PTGDS|27306:HPGDS|8644:AKR1C3|5740:PTGIS|6916:TBXAS1|9536:PTGES|80142:PTGES2|873:CBR1|874:CBR3|247:ALOX15B|1571:CYP2E1|113612:CYP2U1|1579:CYP4A11|284541:CYP4A22|1555:CYP2B6|2053:EPHX2|10728:PTGES3|11283:CYP4F8|126410:CYP4F22|127281:FAM213B	Diaphyseal dysplasia with anemia (Ghosal)|Lamellar ichthyosis (LI) and Non-bullous congenital ichthyosiform erythroderma (NBCIE)|Neurodegeneration with brain iron accumulation (NBIA)	Aspirin (JP16/USP)|Naproxen (JP16/USP/INN)|Sulindac (JP16/USP/INN)|Ibuprofen (JP16/USP/INN)|Piroxicam (JP16/USP/INN)|Diflunisal (JAN/USP/INN)|Ketoprofen (JP16/USP/INN)|Indometacin (JP16/INN)|Mefenamic acid (JP16/USP/INN)|Tolmetin sodium (JAN/USP)|Meclofenamate sodium (USP)|Etodolac (JP16/USP/INN)|Flurbiprofen (JP16/USP/INN)|Zileuton (USP/INN)|Nabumetone (JP16/USP/INN)|Sasapyrine (JAN)|Oxaprozin (JP16/USAN/INN)|Phenylbutazone (JP16/USP/INN)|Sodium salicylate (JP16/USP)|Celecoxib (JAN/USAN/INN)|Rofecoxib (JAN/USAN/INN)|Choline salicylate (JAN/USAN/INN)|Ketorolac tromethamine (USP)|Magnesium salicylate (USP)|Diclofenac potassium (USAN)|Diclofenac sodium (JP16/USP)|Fenoprofen calcium (JAN/USP)|Meloxicam (JAN/USAN/INN)|Naproxen sodium (USP)|Nimesulide (JAN/INN)|Ibuprofen piconol (JAN/USAN)|Tolfenamic acid (JAN/INN)|Trapidil (JP16/INN)|Floctafenine (JAN/USAN/INN)|Tiaprofenic acid (JAN/INN)|Ampiroxicam (JAN/INN)|Benzydamine hydrochloride (JAN/USAN)|Flurbiprofen axetil (JAN)|Alminoprofen (JP16/INN)|Zaltoprofen (JP16/INN)|Indometacin farnesil (JAN)|Pranoprofen (JP16/INN)|Flufenamic acid (JAN/USAN/INN)|Acemetacin (JP16/INN)|Ozagrel hydrochloride hydrate (JAN)|Ozagrel sodium (JP16)|Loxoprofen sodium hydrate (JP16)|Mofezolac (JAN/INN)|Proglumetacin maleate (JAN)|Tenoxicam (JAN/USAN/INN)|Oxatomide (JAN/USAN/INN)|Amfenac sodium hydrate (JAN)|Salicylamide (JAN/USP/INN)|Lornoxicam (JAN/USAN/INN)|Tilmacoxib (JAN/USAN/INN)|Indometacin sodium (JAN)|Flurbiprofen sodium (USP)|Meclofenamic acid (USAN/INN)|Fenoprofen (USAN/INN)|Tolmetin (USAN/INN)|Valdecoxib (USAN/INN)|Atreleuton (USAN/INN)|Benoxaprofen (USAN/INN)|Flufenamate aluminum (JAN)|Darbufelone mesylate (USAN)|Dazmegrel (USAN/INN)|Dazoxiben hydrochloride (USAN)|Etoricoxib (USAN/INN)|Firocoxib (USAN/INN)|Lumiracoxib (USAN/INN)|Dexibuprofen (USAN/INN)|Parecoxib (USAN/INN)|Parecoxib sodium (USAN)|Dexibuprofen lysine (USAN)|Docebenone (USAN/INN)|Enazadrem phosphate (USAN)|Fenleuton (USAN/INN)|Furegrelate sodium (USAN)|Ibuprofen aluminum (USAN)|Lonapalene (USAN)|Aspirin aluminum (JP16)|Pirmagrel (USAN/INN)|Piroxicam betadex (USAN)|Piroxicam cinnamate (USAN)|Piroxicam olamine (USAN)|Ridogrel (USAN/INN)|Ibuprofen lysine (USAN)|Dexketoprofen (INN)|Aloxiprin (INN)|Amfenac (INN)|Benzydamine (INN)|Benzydamine salicylate|Aspirin calcium salt|Aspirin DL-lysine (JAN)|Aspirin magnesium salt|Aspirin sodium|Diclofenac (INN)|Diclofenac diethylamine|Diclofenac hydroxyethylpyrrolidine|Diclofenac calcium|Ibuprofen arginine salt|Ibuprofen sodium|Ketoprofen lysine|Ketoprofen sodium|Ketorolac (INN)|Loxoprofen (INN)|Ozagrel (INN)|Phenylbutazone calcium|Phenylbutazone sodium|Piketoprofen (INN)|Piketoprofen hydrochloride|Proglumetacin (INN)|Ibuprofen sodium (USAN)|Naproxen etemesil (USAN)	
hsa05110	Vibrio cholerae infection - Homo sapiens (human)	Human Diseases; Infectious Diseases	523:ATP6V1A|526:ATP6V1B2|525:ATP6V1B1|528:ATP6V1C1|245973:ATP6V1C2|51382:ATP6V1D|529:ATP6V1E1|90423:ATP6V1E2|9296:ATP6V1F|9550:ATP6V1G1|534:ATP6V1G2|127124:ATP6V1G3|8992:ATP6V0E1|155066:ATP6V0E2|535:ATP6V0A1|50617:ATP6V0A4|23545:ATP6V0A2|10312:TCIRG1|9114:ATP6V0D1|245972:ATP6V0D2|51606:ATP6V1H|537:ATP6AP1|527:ATP6V0C|533:ATP6V0B|10945:KDELR1|11014:KDELR2|11015:KDELR3|9601:PDIA4|30001:ERO1L|55176:SEC61A2|29927:SEC61A1|10952:SEC61B|23480:SEC61G|375:ARF1|2778:GNAS|109:ADCY3|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|1080:CFTR|3784:KCNQ1|6558:SLC12A2|60:ACTB|71:ACTG1|5335:PLCG1|5336:PLCG2|5579:PRKCB|5578:PRKCA|5582:PRKCG|7082:TJP1|9414:TJP2|4583:MUC2	Cholera		Cholera toxin (CTX) is one of the main virulence factors of Vibrio cholerae. Once secreted, CTX B-chain (CTXB) binds to ganglioside GM1 on the surface of the host's cells. After binding takes place, the entire CTX complex is carried from plasma membrane (PM) to endoplasmic reticulum (ER). In the ER, the A-chain (CTXA) is recognized by protein disulfide isomerase (PDI), unfolded, and delivered to the membrane where the membrane-associated ER-oxidase, Ero1, oxidizes PDI to release the CTXA into the protein-conducting channel, Sec61. CTXA is then retro-translocated to the cytosol and induces water and electrolyte secretion by increasing cAMP levels via adenylate cyclase (AC) to exert toxicity.|Other than CTX, Vibrio cholerae generates several toxins that are perilous to eukaryotic cells. Zonula occludens toxin (ZOT) causes tight junction disruption through protein kinase C-dependent actin polymerization. RTX toxin (RtxA) causes actin depolymerization by covalently cross-linking actin monomers into dimers, trimers, and higher multimers. Vibrio cholerae cytolysin (VCC) is an important pore-forming toxin. The assembly of VCC anion channels in cells cause vacuolization and lysis.
hsa04976	Bile secretion - Homo sapiens (human)	Organismal Systems; Digestive System	2052:EPHX1|6579:SLCO1A2|10599:SLCO1B1|28234:SLCO1B3|6554:SLC10A1|10864:SLC22A7|9376:SLC22A8|6580:SLC22A1|3156:HMGCR|949:SCARB1|3949:LDLR|57552:NCEH1|1581:CYP7A1|9971:NR1H4|6256:RXRA|8431:NR0B2|6822:SULT2A1|10998:SLC27A5|570:BAAT|366:AQP9|343:AQP8|64240:ABCG5|64241:ABCG8|8647:ABCB11|1244:ABCC2|9429:ABCG2|6522:SLC4A2|5243:ABCB1|5244:ABCB4|6548:SLC9A1|57835:SLC4A5|8714:ABCC3|10257:ABCC4|200931:OSTalpha|123264:OSTBETA|3781:KCNN2|476:ATP1A1|480:ATP1A4|478:ATP1A3|477:ATP1A2|481:ATP1B1|482:ATP1B2|483:ATP1B3|23439:ATP1B4|486:FXYD2|6344:SCTR|2778:GNAS|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|1080:CFTR|8671:SLC4A4|361:AQP4|358:AQP1|6555:SLC10A2|6523:SLC5A1|6550:SLC9A3|6513:SLC2A1|1576:CYP3A4|7363:UGT2B4|760:CA2	Hyperbilirubinemia|Familial cholestasis|Primary torsion dystonia (PTD)|GLUT1 deficiency syndrome (GLUT1DS)|Hereditary pancreatitis|Primary bile acid malabsorption	Pravastatin sodium (JP16/USAN)	Bile is a vital secretion, essential for digestion and absorption of fats and fat-soluble vitamins in the small intestine. Moreover, bile is an important route of elimination for excess cholesterol and many waste product, bilirubin, drugs and toxic compounds. Bile secretion depends on the function of membrane transport systems in hepatocytes and cholangiocytes and on the structural and functional integrity of the biliary tree. The hepatocytes generate the so-called primary bile in their canaliculi.  Cholangiocytes modify the canalicular bile by secretory and reabsorptive processes as bile passes through the bile ducts. The main solutes in bile are bile acids, which stimulate bile secretion osmotically, as well as facilitate the intestinal absorption of dietary lipids by their detergent properties. Bile acids are also important signalling molecules. Through the activation of nuclear receptors, they regulate their own synthesis and transport rates.
hsa00740	Riboflavin metabolism - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	55312:RFK|80308:FLAD1|5169:ENPP3|5167:ENPP1|52:ACP1|54:ACP5|51205:ACP6|53:ACP2|55:ACPP|93650:ACPT|645:BLVRB|7299:TYR	Generalized arterial calcification of infancy|Acid phosphatase deficiency		
hsa05330	Allograft rejection - Homo sapiens (human)	Human Diseases; Immune Diseases	3133:HLA-E|3134:HLA-F|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|941:CD80|942:CD86|940:CD28|3592:IL12A|3593:IL12B|356:FASLG|355:FAS|5551:PRF1|3002:GZMB|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|3558:IL2|959:CD40LG|958:CD40|3458:IFNG|7124:TNF|3565:IL4|3567:IL5|3586:IL10|100132941:uncharacterized|100291917:uncharacterized	Allograft rejection		Allograft rejection is the consequence of the recipient's alloimmune response to nonself antigens expressed by donor tissues. After transplantation of organ allografts, there are two pathways of antigen presentation. In the direct pathway, recipient T cells react to intact allogeneic MHC molecules expressed on the surface of donor cells. This pathway would activate host CD4 or CD8 T cells. In contrast, donor MHC molecules (and all other proteins) shed from the graft can be taken up by host APCs and presented to recipient T cells in the context of self-MHC molecules - the indirect pathway. Such presentation activates predominantly CD4 T cells. A direct cytotoxic T-cell attack on graft cells can be made only by T cells that recognize the graft MHC molecules directly. Nontheless, T cells with indirect allospecificity can contribute to graft rejection by activating macrophages, which cause tissue injury and fibrosis, and are also likely to be important in the development of an alloantibody response to graft.
hsa00340	Histidine metabolism - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	3034:HAL|131669:UROC1|144193:AMDHD1|10841:FTCD|3067:HDC|1644:DDC|26:ABP1|219:ALDH1B1|224:ALDH3A2|217:ALDH2|501:ALDH7A1|223:ALDH9A1|443:ASPA|91703:ACY3|3176:HNMT|4129:MAOB|4128:MAOA|222:ALDH3B2|220:ALDH1A3|221:ALDH3B1|218:ALDH3A1|57571:CARNS1|55748:CNDP2|84735:CNDP1|51409:HEMK1|131965:METTL6|55798:METTL2B|114049:WBSCR22	Histidinemia|Brunner syndrome|Tourette syndrome	Cyanamide (JP16)|Disulfiram (JP16/USP/INN)|Isoniazid (JP16/USP/INN)|Methyldopa hydrate (JP16)|Phenelzine sulfate (USP)|Carbidopa hydrate (JP16)|Selegiline hydrochloride (JAN/USP)|Tranylcypromine sulfate (USP XXI)|Lazabemide hydrochloride (JAN/USAN)|Amezinium metilsulfate (JAN)|Isoniazid calcium pyruvinate (JAN)|Benserazide hydrochloride (JP16)|Safrazine hydrochloride (JAN)|Isoniazid sodium methanesulfonate hydrate (JAN)|Toloxatone (INN)|Brofaromine (INN)|Moclobemide (USAN/INN)|Rasagiline mesylate (USAN)|Befloxatone (INN)|Pargyline hydrochloride (USAN)|Iproniazid (INN)|Isocarboxazid (INN)|Cimoxatone (INN)|Benserazide (USAN/INN)|Brocresine (USAN/INN)|Ladostigil tartrate (USAN)|Clorgiline (INN)|Caroxazone (USAN/INN)|Selegiline (USAN/INN)|Mofegiline hydrochloride (USAN)|Lazabemide (USAN/INN)|Milacemide hydrochloride (USAN)|Nialamide (INN)|Iproclozide (INN)|Iproniazid phosphate|Methyldopa (INN)|Phenelzine (BAN)|Pargyline (INN)|Rasagiline (USAN/INN)|Tranylcypromine (INN)	
hsa00983	Drug metabolism - other enzymes - Homo sapiens (human)	Metabolism; Xenobiotics Biodegradation and Metabolism	3251:HPRT1|3615:IMPDH2|3614:IMPDH1|8833:GMPS|7172:TPMT|7498:XDH|3704:ITPA|1066:CES1|8824:CES2|7363:UGT2B4|574537:UGT2A2|7367:UGT2B17|7365:UGT2B10|7364:UGT2B7|7366:UGT2B15|54577:UGT1A7|10720:UGT2B11|54490:UGT2B28|54579:UGT1A5|54659:UGT1A3|54657:UGT1A4|54578:UGT1A6|54576:UGT1A8|54600:UGT1A9|10941:UGT2A1|54575:UGT1A10|79799:UGT2A3|54658:UGT1A1|2990:GUSB|1551:CYP3A7|1577:CYP3A5|64816:CYP3A43|1576:CYP3A4|978:CDA|1890:TYMP|1806:DPYD|1807:DPYS|51733:UPB1|1549:CYP2A7|1548:CYP2A6|1553:CYP2A13|151531:UPP2|7378:UPP1|54963:UCKL1|7371:UCK2|83549:UCK1|7084:TK2|7083:TK1|7372:UMPS|9:NAT1|10:NAT2	Dihydropyrimidine dehydrogenase deficiency|Dihydropyrimidinase deficiency|Beta-ureidopropionase deficiency|Thiopurine S-methyltransferase deficiency (TPMT deficiency)	Mycophenolate mofetil (JAN/USAN)|Febuxostat (JAN/USAN/INN)|Gimeracil (JAN/INN)|Oxypurinol (USAN)|Merimepodib (USAN/INN)|Mycophenolate mofetil hydrochloride (USAN)|Mycophenolate sodium (USAN)	
hsa05221	Acute myeloid leukemia - Homo sapiens (human)	Human Diseases; Cancers	3815:KIT|2322:FLT3|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|1147:CHUK|3551:IKBKB|8517:IKBKG|4790:NFKB1|5970:RELA|572:BAD|2475:MTOR|1978:EIF4EBP1|6199:RPS6KB2|6198:RPS6KB1|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|4893:NRAS|3845:KRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|6774:STAT3|6776:STAT5A|6777:STAT5B|5292:PIM1|11040:PIM2|861:RUNX1|862:RUNX1T1|5371:PML|5914:RARA|7704:ZBTB16|1050:CEBPA|6688:SPI1|3728:JUP|6932:TCF7|83439:TCF7L1|6934:TCF7L2|51176:LEF1|595:CCND1|4609:MYC|5467:PPARD|8900:CCNA1	Acute myeloid leukemia (AML)		Acute myeloid leukemia (AML) is a disease that is characterized by uncontrolled proliferation of clonal neoplastic cells and accumulation in the bone marrow of blasts with an impaired differentiation program. AML accounts for approximately 80% of all adult leukemias and remains the most common cause of leukemia death. Two major types of genetic events have been described that are crucial for leukemic transformation. A proposed necessary first event is disordered cell growth and upregulation of cell survival genes. The most common of these activating events were observed in the RTK Flt3, in N-Ras and K-Ras, in Kit, and sporadically in other RTKs. Alterations in myeloid transcription factors governing hematopoietic differentiation provide second necessary event for leukemogenesis. Transcription factor fusion proteins such as AML-ETO, PML-RARalpha or PLZF-RARalpha block myeloid cell differentiation by repressing target genes. In other cases,  the transcription factors themselves are mutated.
hsa00460	Cyanoamino acid metabolism - Homo sapiens (human)	Metabolism; Metabolism of Other Amino Acids	57733:GBA3|2678:GGT1|2686:GGT7|2687:GGT5|124975:GGT6|6470:SHMT1|6472:SHMT2			
hsa00360	Phenylalanine metabolism - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	5053:PAH|1644:DDC|314:AOC2|8639:AOC3|4129:MAOB|4128:MAOA|222:ALDH3B2|220:ALDH1A3|221:ALDH3B1|218:ALDH3A1|10249:GLYAT|2805:GOT1|2806:GOT2|6898:TAT|259307:IL4I1|3242:HPD|4282:MIF|9588:PRDX6	Tyrosinemia	Isoniazid (JP16/USP/INN)|Methyldopa hydrate (JP16)|Phenelzine sulfate (USP)|Carbidopa hydrate (JP16)|Selegiline hydrochloride (JAN/USP)|Tranylcypromine sulfate (USP XXI)|Lazabemide hydrochloride (JAN/USAN)|Amezinium metilsulfate (JAN)|Isoniazid calcium pyruvinate (JAN)|Benserazide hydrochloride (JP16)|Safrazine hydrochloride (JAN)|Isoniazid sodium methanesulfonate hydrate (JAN)|Toloxatone (INN)|Brofaromine (INN)|Moclobemide (USAN/INN)|Rasagiline mesylate (USAN)|Befloxatone (INN)|Pargyline hydrochloride (USAN)|Iproniazid (INN)|Isocarboxazid (INN)|Cimoxatone (INN)|Benserazide (USAN/INN)|Ladostigil tartrate (USAN)|Clorgiline (INN)|Caroxazone (USAN/INN)|Selegiline (USAN/INN)|Mofegiline hydrochloride (USAN)|Lazabemide (USAN/INN)|Milacemide hydrochloride (USAN)|Nitisinone (JAN/USAN/INN)|Nialamide (INN)|Iproclozide (INN)|Iproniazid phosphate|Methyldopa (INN)|Phenelzine (BAN)|Pargyline (INN)|Rasagiline (USAN/INN)|Tranylcypromine (INN)	
hsa04122	Sulfur relay system - Homo sapiens (human)	Genetic Information Processing; Folding, Sorting and Degradation	9054:NFS1|4357:MPST|7263:TST|81605:URM1|27304:MOCS3|90353:CTU1|348180:CTU2|55687:TRMU|4338:MOCS2|4337:MOCS1	Xanthinuria		Ubiquitin and ubiquitin-like proteins (Ubls) are signalling messengers that control many cellular functions, such as cell proliferation, apoptosis, and DNA repair. It is suggested that Ub-protein modification evolved from prokaryotic sulfurtransfer systems. Molybdenum cofactor (Moco) and thiamin are sulfur-containing cofactors whose biosynthesis includes a key sulfur transfer step that uses unique sulfur carrier proteins, MoaD and ThiS. Ubiquitin, MoaD, and ThiS are all structurally related proteins whose C-termini are activated through adenylation by homologous E1-like enzymes. s2T biosynthesis may share similar chemistry with Moco and thiamin synthesis. In Saccharomyces cerevisiae, Urm1 and Uba4 function as part of a ubl protein conjugation system, though they have sequence homology to bacterial sulfur-transfer enzymes and the ability to function in sulfur transfer.
hsa04370	VEGF signaling pathway - Homo sapiens (human)	Environmental Information Processing; Signal Transduction	3791:KDR|9047:SH2D2A|5335:PLCG1|5336:PLCG2|5579:PRKCB|5578:PRKCA|5582:PRKCG|8877:SPHK1|56848:SPHK2|3265:HRAS|3845:KRAS|4893:NRAS|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|4776:NFATC4|4772:NFATC1|4773:NFATC2|4775:NFATC3|10725:NFAT5|5743:PTGS2|5747:PTK2|5829:PXN|998:CDC42|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|9261:MAPKAPK2|7867:MAPKAPK3|3315:HSPB1|6714:SRC|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5879:RAC1|5880:RAC2|5881:RAC3|207:AKT1|208:AKT2|10000:AKT3|842:CASP9|572:BAD|25759:SHC2|4846:NOS3|7422:VEGFA	PTEN hamartoma tumor syndrome (PHTS)|Distal hereditary motor neuropathies (dHMN)	Aspirin (JP16/USP)|Naproxen (JP16/USP/INN)|Sulindac (JP16/USP/INN)|Ibuprofen (JP16/USP/INN)|Piroxicam (JP16/USP/INN)|Diflunisal (JAN/USP/INN)|Ketoprofen (JP16/USP/INN)|Indometacin (JP16/INN)|Mefenamic acid (JP16/USP/INN)|Tolmetin sodium (JAN/USP)|Meclofenamate sodium (USP)|Etodolac (JP16/USP/INN)|Flurbiprofen (JP16/USP/INN)|Nabumetone (JP16/USP/INN)|Sasapyrine (JAN)|Oxaprozin (JP16/USAN/INN)|Phenylbutazone (JP16/USP/INN)|Sodium salicylate (JP16/USP)|Celecoxib (JAN/USAN/INN)|Rofecoxib (JAN/USAN/INN)|Axitinib (JAN/USAN)|Bosutinib (USAN)|Dasatinib (INN)|Pegaptanib sodium (JAN/USAN)|Ranibizumab (genetical recombination) (JAN)|Semaxanib (USAN/INN)|Sorafenib tosilate (JAN)|Vatalanib (USAN/INN)|Sunitinib malate (JAN/USAN)|Vandetanib (JAN/USAN/INN)|Bevacizumab (genetical recombination) (JAN)|Dasatinib hydrate (JAN)|Motesanib|Dexketoprofen (INN)|Ketoprofen sodium|Piketoprofen (INN)|Piketoprofen hydrochloride|Sorafenib (USAN/INN)|Sunitinib (INN)|Bevasiranib sodium (USAN)|Cediranib (USAN/INN)|Cediranib maleate (JAN/USAN)|Motesanib diphosphate (USAN)|Aflibercept (genetical recombination) (JAN)|Tivozanib (USAN/INN)|Bosutinib hydrate (JAN)|Naproxen etemesil (USAN)|Cabozantinib (USAN)	There is now much evidence that VEGFR-2 is the major mediator of VEGF-driven responses in endothelial cells and it is considered to be a crucial signal transducer in both physiologic and pathologic angiogenesis. The binding of VEGF to VEGFR-2 leads to a cascade of different signaling pathways, resulting in the up-regulation of genes involved in mediating the proliferation and migration of endothelial cells and promoting their survival and vascular permeability. For example, the binding of VEGF to VEGFR-2 leads to dimerization of the receptor, followed by intracellular activation of the PLCgamma;PKC-Raf kinase-MEK-mitogen-activated protein kinase (MAPK) pathway and subsequent initiation of DNA synthesis and cell growth, whereas activation of the phosphatidylinositol 3' -kinase (PI3K)-Akt pathway leads to increased endothelial-cell survival. Activation of PI3K, FAK, and p38 MAPK is implicated in cell migration signaling.
hsa04140	Regulation of autophagy - Homo sapiens (human)	Cellular Processes; Transport and Catabolism	3630:INS|5562:PRKAA1|5563:PRKAA2|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3458:IFNG|8408:ULK1|25989:ULK3|9706:ULK2|30849:PIK3R4|8678:BECN1|5289:PIK3C3|9140:ATG12|10533:ATG7|9474:ATG5|23710:GABARAPL1|11345:GABARAPL2|11337:GABARAP|23192:ATG4B|84938:ATG4C|84971:ATG4D|115201:ATG4A|64422:ATG3		Buformin (USAN/INN)|Metformin hydrochloride (JP16/USP)|Buformin hydrochloride (JP16)|Dapiclermin (USAN/INN)|Metformin (USAN/INN)	
hsa05130	Pathogenic Escherichia coli infection - Homo sapiens (human)	Human Diseases; Infectious Diseases	7100:TLR5|929:CD14|7099:TLR4|23643:LY96|112714:TUBA3E|10376:TUBA1B|113457:TUBA3D|7846:TUBA1A|7278:TUBA3C|51807:TUBA8|84790:TUBA1C|79861:TUBAL3|7277:TUBA4A|10383:TUBB4B|10382:TUBB4A|7280:TUBB2A|10381:TUBB3|81027:TUBB1|84617:TUBB6|203068:TUBB|347733:TUBB2B|347688:TUBB8|9181:ARHGEF2|387:RHOA|6093:ROCK1|9475:ROCK2|8440:NCK2|4690:NCK1|7454:WAS|8976:WASL|10095:ARPC1B|10552:ARPC1A|10109:ARPC2|10094:ARPC3|10093:ARPC4|10092:ARPC5|81873:ARPC5L|60:ACTB|71:ACTG1|2534:FYN|25:ABL1|3059:HCLS1|2017:CTTN|4691:NCL|3688:ITGB1|998:CDC42|100506658:OCLN|7430:EZR|999:CDH1|1499:CTNNB1|10971:YWHAQ|3875:KRT18|5578:PRKCA|7534:YWHAZ|9076:CLDN1	Enterohemorrhagic Escherichia coli (EHEC) infection|Enteropathogenic Escherichia coli (EPEC) infection		Enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC) are closely related pathogenic strains of Escherichia coli. The hallmark of EPEC/EHEC infections [DS:H00278 H00277] is induction of attaching and effacing (A/E) lesions that damage intestinal epithelial cells. The capacity to form A/E lesions is encoded mainly by the locus of enterocyte effacement (LEE) pathogenicity island. Tir, Map, EspF, EspG are known LEE-encoded effector proteins secreted via the type III secretion system, which is also LEE-encoded, into the host cell. EPEC and EHEC Tir's link the extracellular bacterium to the cell cytoskeleton. Map and EspF are involved in mitochondrion membrane permeabilization. EspG interacts with tubulins and stimulates microtubule destabilization. LEE-encoded adhesin or intimin (Eae) is exported via the general secretory pathway to the periplasm, where it is inserted into the outer membrane. In addition to Tir, two potential host cell-carried intimin receptors, beta1 integrin (ITGB1) and nucleolin (NCL), have so far been identified. The distinguishing feature of EHEC is the elaboration of Shiga-like toxin (Stx). Stx cleaves ribosomal RNA, thereby disrupting protein synthesis and killing the intoxicated epithelial or endothelial cells.
hsa04964	Proximal tubule bicarbonate reclamation - Homo sapiens (human)	Organismal Systems; Excretory System	6550:SLC9A3|358:AQP1|8671:SLC4A4|476:ATP1A1|480:ATP1A4|478:ATP1A3|477:ATP1A2|481:ATP1B1|482:ATP1B2|483:ATP1B3|23439:ATP1B4|486:FXYD2|10991:SLC38A3|2744:GLS|27165:GLS2|2746:GLUD1|2747:GLUD2|1468:SLC25A10|4190:MDH1|5106:PCK2|5105:PCK1|760:CA2|762:CA4	Combined proximal and distal renal tubular acidosis (RTA type 3)|Proximal renal tubular acidosis (RTA type 2)|Alternating hemiplegia of childhood	Deslanoside (JP16/USP/INN)|Proscillaridin (JAN/USAN/INN)|Lanatoside C (JP16/INN)|Metildigoxin (JP16)|Acetyldigitoxin (INN)|Gitoformate (INN)|Acetyldigoxin	One of the major tasks of the renal proximal tubule (PT) is to secrete acid into the tubule lumen, thereby reabsorbing approximately 80% of the filtered bicarbonate (HCO3(-)), as well as generating "new HCO3(-)" for regulating blood pH. In the tubular lumen, filtered HCO3(-) combines with H(+) in a reaction catalyzed by CA IV. The CO2 thus produced rapidly diffuses into the tubular cells and is combined with water to produce intracellular H(+) and HCO3(-), catalyzed by soluble cytoplasmic CA II. HCO3(-) is then cotransported with Na(+) into blood via the NBC-1. The intracellular H(+) produced by CA II is secreted into the tubular lumen predominantly via the NHE-3. The PT creates the "new HCO3(-)" by taking glutamine and metabolizing it to two molecules each of NH4(+) and HCO3(-). The NH4(+) is excreted into the tubular lumen, and the HCO3(-) , which is "new HCO3(-) ," is returned to the blood, where it replaces the HCO3(-) lost earlier in the titration of nonvolatile acids.
hsa04664	Fc epsilon RI signaling pathway - Homo sapiens (human)	Organismal Systems; Immune System	100132941:uncharacterized|100291917:uncharacterized|2205:FCER1A|2206:MS4A2|2207:FCER1G|6850:SYK|4067:LYN|695:BTK|3635:INPP5D|5335:PLCG1|5336:PLCG2|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5163:PDK1|207:AKT1|208:AKT2|10000:AKT3|5879:RAC1|5880:RAC2|5881:RAC3|6416:MAP2K4|5609:MAP2K7|5606:MAP2K3|5608:MAP2K6|5602:MAPK10|5601:MAPK9|5599:MAPK8|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|3565:IL4|3596:IL13|3562:IL3|3567:IL5|1437:CSF2|7124:TNF|3937:LCP2|10451:VAV3|7409:VAV1|7410:VAV2|2534:FYN|9846:GAB2|27040:LAT|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|5578:PRKCA|5579:PRKCB|5580:PRKCD|5581:PRKCE	Neurodegeneration with brain iron accumulation (NBIA)	Golimumab (genetical recombination) (JAN)|Omalizumab (genetical recombination) (JAN)	Fc epsilon RI-mediated signaling pathways in mast cells are initiated by the interaction of antigen (Ag) with IgE bound to the extracellular domain of the alpha chain of Fc epsilon RI. The activation pathways are regulated both positively and negatively by the interactions of numerous signaling molecules. Mast cells that are thus activated release preformed granules which contain biogenic amines (especially histamines) and proteoglycans (especially heparin). The activation of phospholipase A2 causes the release of membrane lipids followed by development of lipid mediators such as leukotrienes (LTC4, LTD4 and LTE4) and prostaglandins (especially PDG2). There is also secretion of cytokines, the most important of which are TNF-alpha, IL-4 and IL-5. These mediators and cytokines contribute to inflammatory responses.
hsa04540	Gap junction - Homo sapiens (human)	Cellular Processes; Cell Communication	2697:GJA1|57369:GJD2|1902:LPAR1|2773:GNAI3|2770:GNAI1|2771:GNAI2|5154:PDGFA|5155:PDGFB|56034:PDGFC|80310:PDGFD|1950:EGF|5156:PDGFRA|5159:PDGFRB|1956:EGFR|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|6714:SRC|10746:MAP3K2|5607:MAP2K5|5598:MAPK7|112714:TUBA3E|10376:TUBA1B|113457:TUBA3D|7846:TUBA1A|7278:TUBA3C|51807:TUBA8|84790:TUBA1C|79861:TUBAL3|7277:TUBA4A|10383:TUBB4B|10382:TUBB4A|7280:TUBB2A|10381:TUBB3|81027:TUBB1|84617:TUBB6|203068:TUBB|347733:TUBB2B|347688:TUBB8|1453:CSNK1D|983:CDK1|7082:TJP1|153:ADRB1|1812:DRD1|2778:GNAS|1813:DRD2|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|3358:HTR2C|3357:HTR2B|3356:HTR2A|2911:GRM1|2915:GRM5|2767:GNA11|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|3708:ITPR1|3709:ITPR2|3710:ITPR3|5579:PRKCB|5578:PRKCA|5582:PRKCG|2982:GUCY1A3|2977:GUCY1A2|2983:GUCY1B3|5593:PRKG2|5592:PRKG1	Early infantile epileptic encephalopathy|Congenital fibrosis of the extraocular muscles (CFEOM)|Syndactyly|Hypomagnesemia	Adrenaline (JP16)|Haloperidol (JP16/USP/INN)|Clozapine (JAN/USP/INN)|Droperidol (JP16/USP/INN)|Thioridazine (USP/INN)|Tiotixene (JAN)|Timolol (USAN)|Triflupromazine (USP/INN)|Risperidone (JP16/USAN/INN)|Olanzapine (JAN/USAN/INN)|Quetiapine fumarate (JAN/USAN)|Prochlorperazine maleate (JP16/USP)|Paclitaxel (JAN/USP/INN)|Prochlorperazine (JAN/USP/INN)|Perphenazine (JP16/USP/INN)|Pimozide (JP16/USP/INN)|Sertindole (USAN/INN)|Mirtazapine (JAN/USAN/INN)|Colchicine (JP16/USP)|Betaxolol hydrochloride (JP16/USP)|Carteolol hydrochloride (JP16/USP)|Timolol maleate (JP16/USP)|Dopamine hydrochloride (JP16/USP)|Ergotamine tartrate (JP16/USP)|Methylergometrine maleate (JP16)|Metoclopramide (JP16/INN)|Ropinirole hydrochloride (JAN/USAN)|Fluphenazine hydrochloride (JAN/USP)|Fluphenazine enanthate (JP16/USP)|Fluphenazine decanoate (JAN/USP)|Loxapine succinate (USP)|Molindone hydrochloride (USP)|Promazine hydrochloride (USP)|Thioridazine hydrochloride (JP16/USP)|Trifluoperazine hydrochloride (JAN/USP)|Triflupromazine hydrochloride (JAN/USP)|Trazodone hydrochloride (JAN/USP)|Levobunolol hydrochloride (JAN/USP)|Flupentixol (INN)|Spiperone (JAN/USAN)|Vinblastine sulfate (JP16/USP)|Bromperidol (JAN/USAN/INN)|Moperone hydrochloride (JAN)|Aripiprazole (JAN/USAN/INN)|Blonanserin (JAN/INN)|Sulpiride (JP16/USAN/INN)|Ritodrine hydrochloride (JP16/USP)|Zotepine (JAN/INN)|Terguride (JAN/INN)|Mianserin hydrochloride (JAN/USAN)|Thioproperazine mesilate (JAN)|Trifluoperazine maleate (JAN)|Lisuride maleate (JAN)|Nemonapride (JAN/INN)|Pipamperone hydrochloride (JAN)|Propericiazine (JAN)|Levomepromazine hydrochloride (JAN/USAN)|Mosapramine hydrochloride (JAN)|Nipradilol (JAN/INN)|Clebopride malate (JP16)|Domperidone (JP16/USAN/INN)|Vindesine sulfate (JAN/USAN)|Haloperidol decanoate (JAN/USAN)|Dimetotiazine mesilate (JAN)|Vinorelbine ditartrate (JAN)|Apomorphine hydrochloride hydrate (JAN)|Prochlorperazine mesilate (JAN)|Setiptiline maleate (JAN)|Timiperone (JAN)|Perphenazine maleate (JP16)|Fluphenazine maleate (JAN)|Docetaxel hydrate (JAN)|Vincristine sulfate (JP16/USP)|Sultopride hydrochloride (JAN)|Dihydroergotamine mesilate (JP16)|Metoclopramide hydrochloride (JAN)|Flupentixol dihydrochloride (JAN)|Levomepromazine maleate (JP16/USAN)|Loxapine (USAN/INN)|Methysergide (USAN/INN)|Ritodrine (USAN/INN)|Ketanserin (USAN/INN)|Clocapramine hydrochloride hydrate (JP16)|Perospirone hydrochloride hydrate (JAN)|Flibanserin (USAN/INN)|Methoxypromazine maleate|Prochlorperazine edisylate (USP)|Thiothixene hydrochloride (USP)|Clopenthixol (USAN)|Pipamperone (USAN/INN)|Moperone (INN)|Trifluperidol (USAN/INN)|Bromperidol decanoate (USAN)|Butaclamol hydrochloride (USAN)|Iloperidone (USAN/INN)|Mazapertine succinate (USAN)|Oxiperomide (USAN/INN)|Piquindone hydrochloride (USAN)|Remoxipride (USAN)|Remoxipride hydrochloride (USAN)|Tiospirone hydrochloride (USAN)|Adatanserin hydrochloride (USAN)|Adrogolide hydrochloride (USAN)|Altanserin tartrate (USAN)|Amesergide (USAN/INN)|Asenapine maleate (USAN)|Becaplermin (USAN/INN)|Bromocriptine (USAN/INN)|Aplindore fumarate (USAN)|Ciladopa hydrochloride (USAN)|Cinanserin hydrochloride (USAN)|Clebopride (USAN)|Zuclopenthixol (INN)|Dopexamine (USAN/INN)|Ecopipam hydrochloride (USAN)|Perphenazine fendizoate (JAN)|Ibopamine (USAN/INN)|Levobetaxolol hydrochloride (USAN)|Lubazodone hydrochloride (USAN)|Perphenazine hydrochloride|Metoclopramide hydrochloride (USAN)|Metopimazine (USAN/INN)|Paclitaxel poliglumex (USAN/INN)|Paliperidone (JAN/USAN/INN)|Paliperidone palmitate (JAN/USAN)|Pelanserin hydrochloride (USAN)|Pizotyline (USAN)|Pramipexole (USAN/INN)|Quinelorane hydrochloride (USAN)|Quinpirole hydrochloride (USAN)|Raclopride C11 (USP)|Ritanserin (USAN/INN)|Rotigotine (JAN/USAN/INN)|Sibenadet hydrochloride (USAN)|Tropanserin hydrochloride (USAN)|Vindesine (USAN/INN)|Bifeprunox mesylate (USAN)|Olanzapine pamoate (USAN)|Pruvanserin (USAN/INN)|Pruvanserin hydrochloride (USAN)|Quinagolide (INN/BAN)|Metergoline (INN)|Levosulpiride (INN)|Apomorphine (BAN)|Betaxolol (INN)|Carteolol (INN)|Clocapramine (INN)|Dihydroergotamine (INN)|Dihydroergotamine tartrate|Dimetotiazine (INN)|Docetaxel (JAN/INN)|Domperidone maleate|Dopamine (INN)|Ergometrine (INN)|Ergotamine (INN)|Flupentixol decanoate|Fluphenazine (INN)|Haloperidol lactate|Ibopamine hydrochloride|Ketanserin tartrate|Levobunolol (INN)|Lisuride (INN)|Methylergometrine (INN)|Mianserin (INN)|Mosapramine (INN)|Nefazodone (INN)|Pergolide (INN)|Perphenazine decanoate|Perphenazine enantate|Pizotifen malate|Quetiapine (INN)|Quinagolide hydrochloride (BAN)|Ropinirole (USAN/INN)|Setiptiline (INN)|Sultopride (INN)|Talipexole (INN)|Thioproperazine (INN)|Tiapride (INN)|Trifluoperazine (INN)|Trifluperidol hydrochloride|Vinblastine (INN)|Vincristine (INN)|Vinorelbine (INN)|Ziprasidone (INN)|Zuclopenthixol acetate|Zuclopenthixol decanoate|Zuclopenthixol dihydrochloride|Cariprazine hydrochloride (JAN/USAN)|Cariprazine (USAN/INN)|Eplivanserin (USAN/INN)	Gap junctions contain intercellular channels that allow direct communication between the cytosolic compartments of adjacent cells. Each gap junction channel is formed by docking of two 'hemichannels', each containing six connexins, contributed by each neighboring cell. These channels permit the direct transfer of small molecules including ions, amino acids, nucleotides, second messengers and other metabolites between adjacent cells. Gap junctional communication is essential for many physiological events, including embryonic development, electrical coupling, metabolic transport, apoptosis, and tissue homeostasis. Communication through Gap Junction is sensitive to a variety of stimuli, including changes in the level of intracellular Ca2+, pH, transjunctional applied voltage and phosphorylation/dephosphorylation processes. This figure represents the possible activation routes of different protein kinases involved in Cx43 and Cx36 phosphorylation.
hsa05031	Amphetamine addiction - Homo sapiens (human)	Human Diseases; Substance Dependence	7054:TH|1644:DDC|6571:SLC18A2|6570:SLC18A1|4129:MAOB|4128:MAOA|6531:SLC6A3|775:CACNA1C|776:CACNA1D|2902:GRIN1|2903:GRIN2A|2904:GRIN2B|2905:GRIN2C|2906:GRIN2D|116443:GRIN3A|116444:GRIN3B|2890:GRIA1|2891:GRIA2|2892:GRIA3|2893:GRIA4|1812:DRD1|5579:PRKCB|5578:PRKCA|5582:PRKCG|6804:STX1A|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|814:CAMK4|2778:GNAS|111:ADCY5|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|84152:PPP1R1B|5501:PPP1CC|5499:PPP1CA|5500:PPP1CB|1385:CREB1|1386:ATF2|468:ATF4|10488:CREB3|64764:CREB3L2|84699:CREB3L3|148327:CREB3L4|90993:CREB3L1|9586:CREB5|1388:ATF6B|2353:FOS|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|3725:JUN|2354:FOSB|23411:SIRT1|23237:ARC|3065:HDAC1|5173:PDYN			Amphetamine is a psychostimulant drug that exerts persistent addictive effects. Most addictive drugs increase extracellular concentrations of dopamine (DA) in nucleus accumbens (NAc) and medial prefrontal cortex (mPFC), projection areas of mesocorticolimbic DA neurons and key components of the "brain reward circuit". Amphetamine achieves this elevation in extracellular levels of DA by promoting efflux from synaptic terminals. Acute administration of amphetamine induces phosphorylation of cAMP response element-binding protein (CREB) and expression of a number of immediate early genes (IEGs), such as c-fos. The IEGs is likely to initiate downstream molecular events, which may have important roles in the induction and maintenance of addictive states. Chronic exposure to amphetamine induces a unique transcription factor delta FosB, which plays an essential role in long-term adaptive changes in the brain.
hsa04514	Cell adhesion molecules (CAMs) - Homo sapiens (human)	Environmental Information Processing; Signaling Molecules and Interaction	965:CD58|914:CD2|941:CD80|940:CD28|942:CD86|1493:CTLA4|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|920:CD4|3133:HLA-E|3134:HLA-F|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|925:CD8A|926:CD8B|29126:CD274|80380:PDCD1LG2|80381:CD276|5133:PDCD1|23308:ICOSLG|29851:ICOS|958:CD40|959:CD40LG|214:ALCAM|923:CD6|3683:ITGAL|3689:ITGB2|10666:CD226|3383:ICAM1|3384:ICAM2|3385:ICAM3|933:CD22|5788:PTPRC|6614:SIGLEC1|6693:SPN|9080:CLDN9|7122:CLDN5|9071:CLDN10|9075:CLDN2|1365:CLDN3|9074:CLDN6|9073:CLDN8|5010:CLDN11|23562:CLDN14|9076:CLDN1|24146:CLDN15|26285:CLDN17|53842:CLDN22|10686:CLDN16|49861:CLDN20|149461:CLDN19|137075:CLDN23|1366:CLDN7|1364:CLDN4|51208:CLDN18|100506658:OCLN|50848:F11R|58494:JAM2|83700:JAM3|90952:ESAM|1003:CDH5|5175:PECAM1|4267:CD99|3684:ITGAM|6404:SELPLG|6403:SELP|3676:ITGA4|3688:ITGB1|3680:ITGA9|7412:VCAM1|3695:ITGB7|8174:MADCAM1|6402:SELL|947:CD34|2734:GLG1|6401:SELE|5817:PVR|5819:PVRL2|5818:PVRL1|25945:PVRL3|1000:CDH2|4685:NCAM2|4684:NCAM1|3897:L1CAM|23705:CADM1|257194:NEGR1|5792:PTPRF|9672:SDC3|6382:SDC1|6385:SDC4|6383:SDC2|3685:ITGAV|3696:ITGB8|8516:ITGA8|9369:NRXN3|9379:NRXN2|9378:NRXN1|54413:NLGN3|57502:NLGN4X|57555:NLGN2|22871:NLGN1|57863:CADM3|4897:NRCAM|1272:CNTN1|5797:PTPRM|6900:CNTN2|23114:NFASC|8506:CNTNAP1|26047:CNTNAP2|9019:MPZL1|4359:MPZ|4099:MAG|999:CDH1|1462:VCAN|3655:ITGA6|1001:CDH3|1002:CDH4|1013:CDH15|4756:NEO1	Syndromic X-linked mental retardation with epilepsy or seizures|Epidermolysis bullosa, junctional|Ectodermal dysplasia, ectrodactyly, and macular dystrophy (EEM syndrome)|Neonatal ichthyosis-sclerosing cholangitis (NISCH) syndrome|Pitt-Hopkins syndrome|Non-syndromic autosomal dominant mental retardation|Hypotrichosis, congenital, with juvenile macular dystrophy|Vitreoretinal degeneration|Band-like calcification with simplified gyration and polymicrogyria (BLC-PMG)|L1 syndrome|Roussy-Levy syndrome|Hypomagnesemia	Alefacept (USAN/INN)|Alicaforsen sodium (USAN)|Abatacept (genetical recombination) (JAN)|Cilengitide (USAN/INN)|Efalizumab (USAN/INN)|Epratuzumab (USAN/INN)|Galiximab (USAN/INN)|Ipilimumab (USAN/INN)|Siplizumab (USAN/INN)|Valategrast hydrochloride (USAN)	Cell adhesion molecules are (glyco)proteins expressed on the cell surface and play a critical role in a wide array of biologic processes that include hemostasis, the immune response, inflammation, embryogenesis, and development of neuronal tissue. There are four main groups: the integrin family, the immunoglobulin superfamily, selectins, and cadherins. Membrane proteins that mediate immune cell–cell interactions fall into different categories, namely those involved in antigen recognition, costimulation and cellular adhesion. Furthermore cell-cell adhesions are important for brain morphology and highly coordinated brain functions such as memory and learning. During early development of the nervous system, neurons elongate their axons towards their targets and establish and maintain synapses through formation of cell-cell adhesions. Cell-cell adhesions also underpin axon-axon contacts and link neurons with supporting schwann cells and oligodendrocytes.
hsa03030	DNA replication - Homo sapiens (human)	Genetic Information Processing; Replication and Repair	6742:SSBP1|246243:RNASEH1|5422:POLA1|23649:POLA2|5557:PRIM1|5558:PRIM2|5424:POLD1|5425:POLD2|10714:POLD3|57804:POLD4|5426:POLE|5427:POLE2|54107:POLE3|56655:POLE4|4171:MCM2|4172:MCM3|4173:MCM4|4174:MCM5|4175:MCM6|4176:MCM7|6117:RPA1|6118:RPA2|29935:RPA4|6119:RPA3|5111:PCNA|5981:RFC1|5982:RFC2|5984:RFC4|5985:RFC5|5983:RFC3|1763:DNA2|10535:RNASEH2A|79621:RNASEH2B|84153:RNASEH2C|2237:FEN1|3978:LIG1			A complex network of interacting proteins and enzymes is required for DNA replication. Generally, DNA replication follows a multistep enzymatic pathway. At the DNA replication fork, a DNA helicase (DnaB or MCM complex) precedes the DNA synthetic machinery and unwinds the duplex parental DNA in cooperation with the SSB or RPA. On the leading strand, replication occurs continuously in a 5 to 3 direction, whereas on the lagging strand, DNA replication occurs discontinuously by synthesis and joining of short Okazaki fragments. In prokaryotes, the leading strand replication apparatus consists of a DNA polymerase (pol III core), a sliding clamp (beta), and a clamp loader (gamma delta complex). The DNA primase (DnaG) is needed to form RNA primers. Normally, during replication of the lagging-strand DNA template, an RNA primer is removed either by an RNase H or by the 5 to 3 exonuclease activity of DNA pol I, and the DNA ligase joins the Okazaki fragments. In eukaryotes, three DNA polymerases (alpha, delta, and epsilon) have been identified. DNA primase forms a permanent complex with DNA polymerase alpha. PCNA and RFC function as a clamp and a clamp loader. FEN 1 and RNase H1 remove the RNA from the Okazaki fragments and DNA ligase I joins the DNA.
hsa05210	Colorectal cancer - Homo sapiens (human)	Human Diseases; Cancers	2932:GSK3B|8312:AXIN1|8313:AXIN2|1499:CTNNB1|10297:APC2|324:APC|6932:TCF7|83439:TCF7L1|6934:TCF7L2|51176:LEF1|332:BIRC5|4609:MYC|595:CCND1|3845:KRAS|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|572:BAD|842:CASP9|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5594:MAPK1|5595:MAPK3|3725:JUN|2353:FOS|5900:RALGDS|5879:RAC1|5880:RAC2|5881:RAC3|387:RHOA|5602:MAPK10|5601:MAPK9|5599:MAPK8|1630:DCC|836:CASP3|26060:APPL1|7040:TGFB1|7042:TGFB2|7043:TGFB3|7046:TGFBR1|7048:TGFBR2|4087:SMAD2|4088:SMAD3|4089:SMAD4|4292:MLH1|4436:MSH2|4437:MSH3|2956:MSH6|581:BAX|596:BCL2|54205:CYCS|7157:TP53	Colorectal cancer|Oligodontia-colorectal cancer syndrome|Mismatch repair deficiency|Juvenile polyposis syndrome|Familial adenomatous polyposis		Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as  microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC).
hsa00900	Terpenoid backbone biosynthesis - Homo sapiens (human)	Metabolism; Metabolism of Terpenoids and Polyketides	38:ACAT1|39:ACAT2|3158:HMGCS2|3157:HMGCS1|3156:HMGCR|4598:MVK|10654:PMVK|4597:MVD|91734:IDI2|3422:IDI1|2224:FDPS|9453:GGPS1|23590:PDSS1|57107:PDSS2|79947:DHDDS|10269:ZMPSTE24|2339:FNTA|2342:FNTB|23463:ICMT|51449:PCYOX1|9986:RCE1	Mevalonate kinase deficiency|Coenzyme Q10 deficiency|HMG-CoA synthase (HMGCS) deficiency	Lovastatin (USP/INN)|Simvastatin (JP16/USP/INN)|Atorvastatin calcium (USAN)|Cerivastatin sodium (JAN/USAN)|Fluvastatin sodium (JAN/USAN)|Pravastatin sodium (JP16/USAN)|Alendronate sodium hydrate (JP16)|Pamidronate disodium hydrate (JAN)|Risedronate sodium (USP)|Pitavastatin calcium (JAN)|Rosuvastatin calcium (JAN/USAN)|Zoledronic acid hydrate (JAN)|Atorvastatin calcium hydrate (JP16)|Sodium risedronate hydrate (JP16)|Crilvastatin (USAN/INN)|Dalvastatin (USAN/INN)|Tenivastatin calcium (USAN)|Ibandronate sodium hydrate (JAN)|Alendronic acid (INN)|Incadronate disodium hydrate (JAN)|Pamidronic acid (INN)|Atorvastatin (INN)|Cerivastatin (INN)|Fluvastatin (INN)|Incadronic acid (INN)|Pravastatin (INN)|Risedronic acid (INN)|Rosuvastatin (INN)|Zoledronic acid (INN)|Minodronic acid hydrate (JAN)	Terpenoids, also known as isoprenoids, are a large class of natural products consisting of isoprene (C5) units. There are two biosynthetic pathways, the mevalonate pathway [MD:M00095] and the non-mevalonate pathway or the MEP/DOXP pathway [MD:M00096], for the terpenoid building blocks: isopentenyl diphosphate (IPP) and dimethylallyl diphosphate (DMAPP). The action of prenyltransferases then generates higher-order building blocks: geranyl diphosphate (GPP), farsenyl diphosphate (FPP), and geranylgeranyl diphosphate (GGPP), which are the precursors of monoterpenoids (C10), sesquiterpenoids (C15), and diterpenoids (C20), respectively. Condensation of these building blocks gives rise to the precursors of sterols (C30) and carotenoids (C40). The MEP/DOXP pathway is absent in higher animals and fungi, but in green plants the MEP/DOXP and mevalonate pathways co-exist in separate cellular compartments. The MEP/DOXP pathway, operating in the plastids, is responsible for the formation of essential oil monoterpenes and linalyl acetate, some sesquiterpenes, diterpenes, and carotenoids and phytol. The mevalonate pathway, operating in the cytosol, gives rise to triterpenes, sterols, and most sesquiterpenes.
hsa05223	Non-small cell lung cancer - Homo sapiens (human)	Human Diseases; Cancers	2272:FHIT|5915:RARB|6256:RXRA|6257:RXRB|6258:RXRG|1029:CDKN2A|1019:CDK4|1021:CDK6|595:CCND1|5925:RB1|1871:E2F3|1869:E2F1|1870:E2F2|3845:KRAS|11186:RASSF1|83593:RASSF5|6789:STK4|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5170:PDPK1|207:AKT1|208:AKT2|10000:AKT3|572:BAD|842:CASP9|2309:FOXO3|1950:EGF|7039:TGFA|1956:EGFR|2064:ERBB2|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|5335:PLCG1|5336:PLCG2|5579:PRKCB|5578:PRKCA|5582:PRKCG|7157:TP53	Non-small cell lung cancer	Gefitinib (JAN/USAN/INN)|Erlotinib hydrochloride (JAN/USAN)|Erlotinib (INN)	Lung cancer is a leading cause of cancer death among men and women in industrialized countries. Non-small-cell lung cancer (NSCLC) accounts for approximately 85% of lung cancer and represents a heterogeneous group of cancers, consisting mainly of squamous cell (SCC), adeno (AC) and large-cell carcinoma. Molecular mechanisms altered in NSCLC include activation of oncogenes, such as K-RAS and c-erbB-2, and inactivation of tumorsuppressor genes, such as p53, p16INK4a, RAR-beta, and RASSF1. Point mutations within the K-RAS gene inactivate GTPase activity and the p21-RAS protein continuously transmits growth signals to the nucleus. Overexpression of c-erbB-2 or EGFR leads to a proliferative advantage. Inactivating mutation of p53 can lead to more rapid proliferation and reduced apoptosis. The protein encoded by the p16INK4a  inhibits formation of CDK-cyclin-D complexes by competitive binding of CDK4 and CDK6. Loss of p16INK4a expression is a common feature of NSCLC. RAR-beta is a nuclear receptor that bears vitamin-A-dependent transcriptional activity. RASSF1A is able to form heterodimers with Nore-1, an RAS effector.Therefore loss of RASSF1A might shift the balance of RAS activity towards a growth-promoting effect.
hsa04310	Wnt signaling pathway - Homo sapiens (human)	Environmental Information Processing; Signal Transduction	64840:PORCN|7471:WNT1|7482:WNT2B|7472:WNT2|7473:WNT3|89780:WNT3A|54361:WNT4|7474:WNT5A|81029:WNT5B|7475:WNT6|7477:WNT7B|7476:WNT7A|7479:WNT8B|7478:WNT8A|7483:WNT9A|7484:WNT9B|7480:WNT10B|80326:WNT10A|7481:WNT11|51384:WNT16|9350:CER1|11197:WIF1|27121:DKK4|27123:DKK2|22943:DKK1|6422:SFRP1|6423:SFRP2|6424:SFRP4|6425:SFRP5|8321:FZD1|8324:FZD7|2535:FZD2|7976:FZD3|8322:FZD4|8325:FZD8|7855:FZD5|8323:FZD6|8326:FZD9|11211:FZD10|4040:LRP6|4041:LRP5|1454:CSNK1E|1856:DVL2|1857:DVL3|1855:DVL1|10023:FRAT1|23401:FRAT2|1459:CSNK2A2|1457:CSNK2A1|1460:CSNK2B|85409:NKD2|85407:NKD1|80319:CXXC4|59343:SENP2|2932:GSK3B|1499:CTNNB1|10297:APC2|324:APC|5518:PPP2R1A|5519:PPP2R1B|5525:PPP2R5A|5528:PPP2R5D|5526:PPP2R5B|5527:PPP2R5C|5529:PPP2R5E|5516:PPP2CB|5515:PPP2CA|1452:CSNK1A1|122011:CSNK1A1L|8312:AXIN1|8313:AXIN2|6932:TCF7|83439:TCF7L1|6934:TCF7L2|51176:LEF1|56998:CTNNBIP1|57680:CHD8|64321:SOX17|1488:CTBP2|1487:CTBP1|1387:CREBBP|2033:EP300|8607:RUVBL1|4087:SMAD2|4088:SMAD3|4089:SMAD4|6885:MAP3K7|51701:NLK|4609:MYC|3725:JUN|8061:FOSL1|595:CCND1|894:CCND2|896:CCND3|5467:PPARD|4316:MMP7|5663:PSEN1|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|7157:TP53|6477:SIAH1|27101:CACYBP|6500:SKP1|6907:TBL1X|90665:TBL1Y|79718:TBL1XR1|23291:FBXW11|8945:BTRC|8454:CUL1|9978:RBX1|57216:VANGL2|81839:VANGL1|144165:PRICKLE1|166336:PRICKLE2|23500:DAAM2|23002:DAAM1|387:RHOA|6093:ROCK1|9475:ROCK2|5879:RAC1|5880:RAC2|5881:RAC3|5602:MAPK10|5601:MAPK9|5599:MAPK8|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|5579:PRKCB|5578:PRKCA|5582:PRKCG|4776:NFATC4|4772:NFATC1|4773:NFATC2|4775:NFATC3|10725:NFAT5|2239:GPC4	Frontotemporal lobar degeneration (FTLD)|Sclerosing bone dysplasias|Osteoporosis-pseudoglioma syndrome (OPPG)|Familial exudative vitreoretinopathy (FEVR)|46,XX disorders of sex development (Disorders of gonadal development)|46,XX disorders of sex development (Other)|46,XY disorders of sex development (Disorders of gonadal development)|Tooth agenesis|Tetra-amelia|Odontoonychodermal dysplasia|Acne inversa|Progressive myoclonic epilepsy (PME)|Oligodontia-colorectal cancer syndrome|Li-Fraumeni syndrome|Caudal duplication anomaly|Pilomatricoma|Focal dermal hypoplasia|Caudal regression syndrome and Sirenomelia|Choroid plexus papilloma|Juvenile polyposis syndrome|Familial adenomatous polyposis|Vesicoureteral reflux		Wnt proteins are secreted morphogens that are required for basic developmental processes, such as cell-fate specification, progenitor-cell proliferation and the control of asymmetric cell division, in many different species and organs. There are at least three different Wnt pathways: the canonical pathway, the planar cell polarity (PCP) pathway and the Wnt/Ca2+ pathway. In the canonical Wnt pathway, the major effect of Wnt ligand binding to its receptor is the stabilization of cytoplasmic beta-catenin through inhibition of the bea-catenin degradation complex. Beta-catenin is then free to enter the nucleus and activate Wnt-regulated genes through its interaction with TCF (T-cell factor) family transcription factors and concomitant recruitment of coactivators. Planar cell polarity (PCP) signaling leads to the activation of the small GTPases RHOA (RAS homologue gene-family member A) and RAC1, which activate the stress kinase JNK (Jun N-terminal kinase) and ROCK (RHO-associated coiled-coil-containing protein kinase 1) and leads to remodelling of the cytoskeleton and changes in cell adhesion and motility. WNT-Ca2+ signalling is mediated through G proteins and phospholipases and leads to transient increases in cytoplasmic free calcium that subsequently activate the kinase PKC (protein kinase C) and CAMKII (calcium calmodulin mediated kinase II) and the phosphatase calcineurin.
hsa00430	Taurine and hypotaurine metabolism - Homo sapiens (human)	Metabolism; Metabolism of Other Amino Acids	1036:CDO1|2571:GAD1|2572:GAD2|51380:CSAD|84890:ADO|2678:GGT1|2686:GGT7|2687:GGT5|124975:GGT6|570:BAAT	Cerebral palsy		
hsa04740	Olfactory transduction - Homo sapiens (human)	Organismal Systems; Sensory System	81168:OR8J3|8388:OR1E2|4992:OR1F1|8390:OR1G1|8387:OR1E1|8590:OR6A2|4993:OR2C1|7932:OR2H2|26689:OR4D1|26493:OR8B8|26716:OR2H1|26658:OR7C2|4994:OR3A1|4991:OR1D2|8392:OR3A3|8383:OR1A1|4995:OR3A2|8386:OR1D5|10798:OR5I1|26686:OR4E2|26189:OR1A2|26707:OR2J2|26212:OR2B6|26648:OR7E24|26735:OR1L3|26531:OR11A1|23538:OR52A1|26496:OR10A3|56656:OR2S2|26737:OR1L1|26529:OR12D2|26219:OR1J4|26248:OR2K2|26532:OR10H3|26339:OR5K1|26245:OR2M4|26692:OR2W1|26533:OR10G3|26188:OR1C1|26538:OR10H2|26534:OR10G2|26492:OR8G2|26740:OR1J2|26338:OR5L2|26211:OR2F1|26539:OR10H1|26494:OR8G1|26333:OR7A17|26476:OR10J1|26696:OR2T1|26246:OR2L2|26659:OR7A5|26682:OR4F4|26664:OR7C1|26683:OR4F3|196335:OR56B4|119764:OR4X2|128371:OR6K6|119695:OR52R1|130075:OR9A4|127623:OR2B11|122742:OR4L1|134083:OR2Y1|135924:OR9A2|81472:OR2C3|120787:OR52W1|120065:OR5P2|120066:OR5P3|219464:OR5T2|219417:OR8U1|79310:OR5H2|219479:OR5R1|219469:OR8H1|119694:OR51F2|81050:OR5AC2|219865:OR8G5|121130:OR10P1|135941:OR2A14|79290:OR13A1|119692:OR51S1|79541:OR2A4|119682:OR51L1|81127:OR4K15|219473:OR8K3|79295:OR5H6|219493:OR5AR1|119687:OR51A7|79317:OR4K5|219874:OR6T1|119765:OR4B1|79501:OR4F5|125962:OR7G1|144124:OR10A5|219437:OR5L1|219858:OR8B12|219982:OR5A1|128372:OR6N1|219436:OR5D14|219958:OR1S2|81448:OR6K2|219954:OR9I1|219957:OR9Q2|127068:OR2T34|120796:OR56A1|120776:OR2D2|219968:OR5B21|81469:OR2G3|138883:OR1N1|158131:OR1Q1|219960:OR10Q1|219875:OR4D5|121364:OR10A7|81309:OR4C15|219447:OR5AS1|81399:OR4F16|127066:OR14C36|219453:OR8K5|81470:OR2G2|162998:OR7D2|81327:OR4A16|79345:OR51B2|79473:OR52N1|219956:OR9Q1|219484:OR5M8|219959:OR1S1|81442:OR6N2|81392:OR2AE1|81696:OR5V1|138803:OR13C3|138804:OR13C4|81797:OR12D3|81318:OR4A5|135946:OR6B1|219952:OR6Q1|143496:OR52B4|126370:OR1I1|119774:OR52K2|138881:OR1L8|219477:OR8J1|119678:OR52E2|119772:OR52M1|143502:OR52I2|81300:OR4P4|125963:OR1M1|138882:OR1N2|127077:OR2T11|127062:OR2M3|126541:OR10H4|120793:OR56A4|127064:OR2T12|127069:OR2T10|219869:OR10G8|135948:OR2F2|127059:OR2M5|127385:OR10J5|120775:OR2D3|128368:OR10Z1|219432:OR4C6|122748:OR11H6|219438:OR5D18|219870:OR10G9|128367:OR10X1|219482:OR5M3|127074:OR2T4|219873:OR10S1|128360:OR10T2|125958:OR7D4|143503:OR51E1|138802:OR13C8|219983:OR4D6|138805:OR13F1|138799:OR13C5|122740:OR4K14|219986:OR4D11|119749:OR4C46|219981:OR5A2|219428:OR4C16|219431:OR4S2|79339:OR51B4|119679:OR52J3|144125:OR2AG1|81285:OR51E2|79544:OR4K1|150681:OR6B3|124538:OR4D2|121275:OR10AD1|219429:OR4C11|81697:OR2B2|81282:OR51G2|81061:OR11H1|81099:OR4F17|219487:OR5M11|79324:OR51G1|341799:OR6S1|390084:OR56A5|120586:OR8I2|283092:OR4C13|403239:OR2T27|343169:OR6F1|346528:OR2A1|390067:OR52H1|219965:OR5B17|393046:OR2A5|392391:OR5C1|283189:OR9G4|341152:OR2AT4|343171:OR2W3|390264:OR10G4|390265:OR10G7|391211:OR2G6|338751:OR52L1|392390:OR1L6|285659:OR2V2|347169:OR1B1|347168:OR1J1|283093:OR4C12|343406:OR10R2|391195:OR2T33|391109:OR10K1|401993:OR2T5|390054:OR52A5|403253:OR4A47|284521:OR2L13|391114:OR6K3|256144:OR4C3|390433:OR4K13|390078:OR52E6|338755:OR2AG2|390436:OR4K17|390079:OR52E8|391191:OR2AK2|390077:OR52N2|401427:OR2A7|401666:OR51A4|390181:OR5AK2|391192:OR2L3|284433:OR10H5|391194:OR2M2|390201:OR10V1|390261:OR6M1|391196:OR2M7|390648:OR4F6|391107:OR10K2|284383:OR2Z1|341276:OR10A2|390093:OR10A6|390063:OR51I1|390260:OR6X1|391112:OR6Y1|390445:OR5AU1|390437:OR4N5|256148:OR4S1|390321:OR6C1|390326:OR6C76|390061:OR51Q1|390064:OR51I2|390195:OR5AN1|390066:OR52D1|390429:OR4N2|402317:OR2A42|390883:OR7G3|390199:OR4D9|391189:OR11L1|347468:OR13H1|391190:OR2L8|282763:OR51B5|392309:OR13J1|392138:OR2A25|390081:OR52E4|390442:OR11H4|284532:OR14A16|390197:OR4D10|286362:OR13C9|392376:OR13C2|392392:OR1K1|390037:OR52I1|390142:OR5D13|390038:OR51D1|286365:OR13D1|390113:OR4X1|81328:OR4A15|441608:OR5B3|441669:OR4Q3|442361:OR2A2|441639:OR9K2|442191:OR14J1|441670:OR4M1|442186:OR2J3|441933:OR13G1|346525:OR2A12|403282:OR6C65|389090:OR6B2|504189:OR8U8|442184:OR2B3|255725:OR52B2|390083:OR56A3|254973:OR1L4|403257:OR4C45|390538:OR4M2|283694:OR4N4|343172:OR2T8|390649:OR4F15|338675:OR5AP2|390191:OR5B12|401992:OR2T2|442194:OR10C1|441911:OR10J3|256892:OR51F1|403284:OR6C68|346517:OR6V1|390162:OR5M9|390151:OR8H2|390152:OR8H3|390155:OR5T1|390154:OR5T3|338674:OR5F1|390157:OR8K1|254783:OR6C74|282770:OR10AG1|387748:OR56B1|282775:OR5J2|283365:OR6C6|401665:OR51T1|390174:OR9G1|343563:OR2T29|390439:OR11G2|390075:OR52N5|390323:OR6C75|390036:OR52K1|390327:OR6C70|341418:OR6C4|283297:OR10A4|343173:OR2T3|390144:OR5D16|401994:OR14I1|390892:OR7A10|254879:OR2T6|402135:OR5K2|390882:OR7G2|390275:OR8A1|254786:OR6C3|390168:OR5M1|283162:OR8B4|341416:OR6C2|390167:OR5M10|338662:OR8D4|390059:OR51M1|390072:OR52N4|341568:OR8S1|390431:OR4K2|340980:OR52B6|283111:OR51V1|283159:OR8D1|283160:OR8D2|401667:OR51A2|390058:OR51B6|2774:GNAL|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|5132:PDC|5593:PRKG2|5592:PRKG1|109:ADCY3|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|2979:GUCA1B|2978:GUCA1A|9626:GUCA1C|1261:CNGA3|1262:CNGA4|1258:CNGB1|1179:CLCA1|9635:CLCA2|22802:CLCA4|157:ADRBK2|3000:GUCY2D|409:ARRB2|5137:PDE1C|100272148:GPCRLTM7|128366:OR6P1|26341:OR5H1|26595:OR8B2|390148:OR5W2|390190:OR5B2|390271:OR8B3|403277:OR5K3|403278:OR5K4|440153:OR11H12|441308:OR4F21|504190:OR8U9|504191:OR9G9|81341:OR10W1			Within the compact cilia of the olfactory receptor neurons (ORNs) a cascade of enzymatic activity transduces the binding of an odorant molecule to a receptor into an electrical signal that can be transmitted to the brain. Odorant molecules bind to a receptor protein (R) coupled to an olfactory specific Gs-protein (G) and activate a type III adenylyl cyclase (AC), increasing intracellular cAMP levels. cAMP targets an olfactory-specific cyclic-nucleotide gated ion channel (CNG), allowing cations, particularly Na and Ca, to flow down their electrochemical gradients into the cell, depolarizing the ORN. Furthermore, the Ca entering the cell is able to activate a Ca-activated Cl channel, which would allow Cl to flow out of the cell, thus further increasing the depolarization. Elevated intracellular Ca causes adaptation by at least two different molecular steps: inhibition of the activity of adenylyl cyclase via CAMKII-dependent phosphorylation and down-regulation of the affinity of the CNG channel to cAMP.Longer exposure to odorants can stimulate particulate guanylyl cyclase in cilia to produce cGMP and activate PKG, leading to a further increase in amount and duration of intracellular cAMP levels, which may serve to convert inactive forms of protein kinase A (PKA2) to active forms (PKA*). As part of a feedback loop, PKA can inhibit the activation of particulate guanylyl cyclase.
hsa04380	Osteoclast differentiation - Homo sapiens (human)	Organismal Systems; Development	1435:CSF1|1436:CSF1R|2885:GRB2|5594:MAPK1|5595:MAPK3|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|3458:IFNG|3459:IFNGR1|3460:IFNGR2|6772:STAT1|3552:IL1A|3553:IL1B|3554:IL1R1|7124:TNF|7132:TNFRSF1A|7040:TGFB1|7042:TGFB2|7046:TGFBR1|7048:TGFBR2|8600:TNFSF11|8792:TNFRSF11A|4982:TNFRSF11B|7186:TRAF2|7189:TRAF6|3932:LCK|2534:FYN|9020:MAP3K14|1147:CHUK|5971:RELB|4791:NFKB2|6885:MAP3K7|10454:TAB1|23118:TAB2|8517:IKBKG|3551:IKBKB|4792:NFKBIA|5970:RELA|4790:NFKB1|3456:IFNB1|5604:MAP2K1|5608:MAP2K6|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|5609:MAP2K7|5602:MAPK10|5601:MAPK9|5599:MAPK8|2353:FOS|2354:FOSB|2355:FOSL2|8061:FOSL1|3725:JUN|3727:JUND|3726:JUNB|5879:RAC1|50508:NOX3|1536:CYBB|27035:NOX1|1535:CYBA|4688:NCF2|653361:NCF1|4689:NCF4|695:BTK|7006:TEC|126014:OSCAR|79168:LILRA6|10288:LILRB2|11006:LILRB4|10990:LILRB5|11025:LILRB3|23547:LILRA4|11027:LILRA2|11026:LILRA3|11024:LILRA1|10859:LILRB1|2209:FCGR1A|2213:FCGR2B|9103:FCGR2C|2212:FCGR2A|2215:FCGR3B|2214:FCGR3A|54209:TREM2|10326:SIRPB1|55423:SIRPG|140885:SIRPA|7305:TYROBP|6850:SYK|29760:BLNK|3937:LCP2|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|814:CAMK4|1385:CREB1|6688:SPI1|4286:MITF|1513:CTSK|54:ACP5|799:CALCR|3690:ITGB3|5468:PPARG|3454:IFNAR1|3455:IFNAR2|3716:JAK1|7297:TYK2|6773:STAT2|10379:IRF9|8651:SOCS1|9021:SOCS3|9846:GAB2|2274:FHL2|1540:CYLD|8878:SQSTM1|4772:NFATC1|4773:NFATC2|5336:PLCG2	Osteopetrosis|Paget's disease of bone and related disorders|Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL)|Osteoporosis, lymphedema, anhydrotic ectodermal dysplasia with immunodeficiency (OLEDAID)|Incontinentia pigmenti|Loeys-Dietz syndrome (LDS)|Cocoon syndrome|Aplastic anemia (AA)|Tietz syndrome	Etanercept (genetical recombination) (JAN)|Interferon beta-1b (genetical recombination) (JAN)|Infliximab (genetical recombination) (JAN)|Anakinra (USAN/INN)|Interferon beta (JAN)|Denosumab (genetical recombination) (JAN)|Interferon beta-1a (genetical recombination) (JAN)	The osteoclasts, multinucleared cells originating from the hematopoietic monocyte-macrophage lineage, are responsible for bone resorption. Osteoclastogenesis is mainly regulated by signaling pathways activated by RANK and immune receptors, whose ligands are expressed on the surface of osteoblasts. Signaling from RANK changes gene expression patterns through transcription factors like NFATc1 and characterizes the active osteoclast.
hsa04340	Hedgehog signaling pathway - Homo sapiens (human)	Environmental Information Processing; Signal Transduction	6469:SHH|3549:IHH|50846:DHH|5727:PTCH1|8643:PTCH2|6608:SMO|27148:STK36|51684:SUFU|2737:GLI3|2736:GLI2|2735:GLI1|7471:WNT1|7482:WNT2B|7472:WNT2|7473:WNT3|89780:WNT3A|54361:WNT4|7474:WNT5A|81029:WNT5B|7475:WNT6|7477:WNT7B|7476:WNT7A|7479:WNT8B|7478:WNT8A|7483:WNT9A|7484:WNT9B|7480:WNT10B|80326:WNT10A|7481:WNT11|51384:WNT16|650:BMP2|652:BMP4|653:BMP5|656:BMP8B|655:BMP7|654:BMP6|353500:BMP8A|64399:HHIP|2619:GAS1|4036:LRP2|51715:RAB23|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|2932:GSK3B|1452:CSNK1A1|122011:CSNK1A1L|1455:CSNK1G2|1456:CSNK1G3|53944:CSNK1G1|1453:CSNK1D|1454:CSNK1E|23291:FBXW11|8945:BTRC|7546:ZIC2	Acrocallosal syndrome|Holoprosencephaly (HPE)|Brachydactyly|Pallister-Hall syndrome|46,XY disorders of sex development (Disorders of gonadal development)|Odontoonychodermal dysplasia|Solitary median maxillary central incisor syndrome|Acrocapitofemoral dysplasia|Triphalangeal thumb|Donnai-Barrow syndrome|Basal cell nevus syndrome|Anophthalmia and microphthalmia (A/M)|Schizencephaly	Vismodegib (USAN/INN)	The Hedgehog (Hh) family of secreted signaling proteins plays a crucial role in development of diverse animal phyla, from Drosophila to humans, regulating morphogenesis of a variety of tissues and organs. Hh signaling is also involved in control of stem cell proliferation in adult tissues and aberrant activation of the Hh pathway has been linked to multiple types of human cancer. Members of the Hh family bind to patched (ptc), thus releasing smoothened (smo) to transduce a signal. Transcriptional activation occurs through the GLI family of proteins resulting in activation of target genes.
hsa05144	Malaria - Homo sapiens (human)	Human Diseases; Infectious Diseases	9672:SDC3|6382:SDC1|6385:SDC4|6383:SDC2|4035:LRP1|975:CD81|3082:HGF|4233:MET|2532:DARC|2993:GYPA|2994:GYPB|2995:GYPC|3039:HBA1|3040:HBA2|3045:HBD|3043:HBB|54106:TLR9|4615:MYD88|7097:TLR2|7099:TLR4|3586:IL10|7040:TGFB1|7042:TGFB2|7043:TGFB3|3576:IL8|3569:IL6|6347:CCL2|1440:CSF3|3553:IL1B|7124:TNF|3592:IL12A|3606:IL18|3820:KLRB1|22914:KLRK1|3458:IFNG|948:CD36|1378:CR1|5175:PECAM1|7412:VCAM1|1311:COMP|7059:THBS3|7058:THBS2|7060:THBS4|7057:THBS1|6401:SELE|3683:ITGAL|3689:ITGB2|3383:ICAM1|959:CD40LG|958:CD40|6403:SELP	Malaria		Plasmodium protozoa are parasites that account for malaria infection. Sporozoite forms of the parasite are injected by mosquito bites under the skin and are carried to the liver where they develop into the merozoite form.|Sporozoite invasion of hepatocytes is mediated by parasite surface protein like CSP. Subsequent infection into red blood cells (RBCs) by merozoites causes malaria disease via aberrant cytokine production and sequestration of parasite-infected red blood cells (pRBCs) to host endothelium. Microvasculature sequestration in the brain brings about cerebral malaria that can results in death or persisting neurological impairment. PfEMP1 has been suggested as the key adhesive molecule of pRBCs.
hsa05132	Salmonella infection - Homo sapiens (human)	Human Diseases; Infectious Diseases	929:CD14|7099:TLR4|3929:LBP|4615:MYD88|7100:TLR5|58484:NLRC4|29108:PYCARD|834:CASP1|5879:RAC1|998:CDC42|391:RHOG|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|5594:MAPK1|5595:MAPK3|5602:MAPK10|5601:MAPK9|5599:MAPK8|2353:FOS|3725:JUN|4790:NFKB1|5970:RELA|3606:IL18|3553:IL1B|3552:IL1A|3569:IL6|3576:IL8|6348:CCL3|6349:CCL3L1|414062:CCL3L3|9560:CCL4L1|388372:CCL4L2|6351:CCL4|2921:CXCL3|2920:CXCL2|2919:CXCL1|1437:CSF2|8936:WASF1|10163:WASF2|7454:WAS|8976:WASL|10092:ARPC5|81873:ARPC5L|10093:ARPC4|10094:ARPC3|10095:ARPC1B|10552:ARPC1A|10109:ARPC2|7082:TJP1|60:ACTB|71:ACTG1|29941:PKN3|5585:PKN1|5586:PKN2|6093:ROCK1|9475:ROCK2|23207:PLEKHM2|3831:KLC1|89953:KLC4|64837:KLC2|147700:KLC3|7879:RAB7A|338382:RAB7B|83547:RILP|1778:DYNC1H1|79659:DYNC2H1|1780:DYNC1I1|1781:DYNC1I2|1783:DYNC1LI2|51143:DYNC1LI1|375189:PFN4|5217:PFN2|5216:PFN1|345456:PFN3|2317:FLNB|2318:FLNC|2316:FLNA|3458:IFNG|3459:IFNGR1|3460:IFNGR2|4843:NOS2|4627:MYH9|4628:MYH10|79784:MYH14	Typhoid fever		Salmonella infection usually presents as a self-limiting gastroenteritis or the more severe typhoid fever and bacteremia. The common disease-causing Salmonella species in human is a single species, Salmonella enterica, which has numerous serovars.|Following intestinal colonization Salmonella inject effector proteins into the host cells using a type III secretion system (T3SS), T3SS1. Then a small group of effector proteins induce rearrangement of the actin cytoskeleton resulting in membrane ruffles and rapid internalization of the bacteria.The T3SS2 is responsible for translocating effector proteins that direct Salmonella-containing vacuole (SCV) maturation. The majority of the bacteria are known to survive and replicate in SCV.
hsa03018	RNA degradation - Homo sapiens (human)	Genetic Information Processing; Folding, Sorting and Degradation	28960:DCPS|51013:EXOSC1|23404:EXOSC2|51010:EXOSC3|22894:DIS3|11340:EXOSC8|118460:EXOSC6|23016:EXOSC7|54512:EXOSC4|56915:EXOSC5|5393:EXOSC9|5394:EXOSC10|10438:C1D|10200:MPHOSPH6|11044:PAPD7|84186:ZCCHC7|23517:SKIV2L2|6499:SKIV2L|9652:TTC37|80349:WDR61|246175:CNOT6L|57472:CNOT6|23019:CNOT1|4848:CNOT2|4849:CNOT3|4850:CNOT4|9337:CNOT8|29883:CNOT7|9125:RQCD1|25904:CNOT10|170506:DHX36|5073:PARN|7832:BTG2|694:BTG1|10950:BTG3|54766:BTG4|10766:TOB2|10140:TOB1|340529:PABPC1L2A|645974:PABPC1L2B|5042:PABPC3|8761:PABPC4|26986:PABPC1|132430:PABPC4L|140886:PABPC5|80336:PABPC1L|9924:PAN2|255967:PAN3|55802:DCP1A|196513:DCP1B|167227:DCP2|1656:DDX6|80153:EDC3|23644:EDC4|219988:PATL1|54464:XRN1|22803:XRN2|27257:LSM1|57819:LSM2|27258:LSM3|25804:LSM4|23658:LSM5|11157:LSM6|51690:LSM7|51691:NAA38|2027:ENO3|2026:ENO2|2023:ENO1|87178:PNPT1|3313:HSPA9|3329:HSPD1			The correct processing, quality control and turnover of cellular RNA molecules are critical to many aspects in the expression of genetic information. In eukaryotes, two major pathways of mRNA decay exist and both pathways are initiated by poly(A) shortening of the mRNA. In the 5' to 3' pathway, this is followed by decapping which then permits the 5' to 3' exonucleolytic degradation of transcripts. In the 3' to 5' pathway, the exosome, a large multisubunit complex, plays a key role. The exosome exists in archaeal cells, too. In bacteria, endoribonuclease E, a key enzyme involved in RNA decay and processing, organizes a protein complex called degradosome. RNase E or R interacts with the phosphate-dependent exoribonuclease polynucleotide phosphorylase, DEAD-box helicases, and additional factors in the RNA-degrading complex.
hsa04973	Carbohydrate digestion and absorption - Homo sapiens (human)	Organismal Systems; Digestive System	277:AMY1B|276:AMY1A|278:AMY1C|280:AMY2B|279:AMY2A|3938:LCT|8972:MGAM|6476:SI|6523:SLC5A1|476:ATP1A1|480:ATP1A4|478:ATP1A3|477:ATP1A2|481:ATP1B1|482:ATP1B2|483:ATP1B3|23439:ATP1B4|486:FXYD2|6514:SLC2A2|3101:HK3|3099:HK2|3098:HK1|80201:HKDC1|2542:SLC37A4|2538:G6PC|57818:G6PC2|6518:SLC2A5|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|207:AKT1|208:AKT2|10000:AKT3|776:CACNA1D|80834:TAS1R2|83756:TAS1R3|346562:GNAT3|5330:PLCB2|5579:PRKCB		Acarbose (JAN/USAN/INN)|Miglitol (JAN/USAN/INN)|Voglibose (JP16/USAN/INN)	Dietary carbohydrate in humans and omnivorous animals is a major nutrient.  The carbohydrates that we ingest vary from the lactose in milk to complex carbohydrates. These carbohydrates are digested to monosaccharides, mostly glucose, galactose and fructose, prior to absorption in the small intestine. Glucose and galactose are initially transported into the enterocyte by SGLT1 located in the apical brush border membrane and then exit through the basolateral membrane by either GLUT2 or exocytosis. In a new model of intestinal glucose absorption, transport by SGLT1 induces rapid insertion and activation of GLUT2 in the brush border membrane by a PKC betaII-dependent mechanism. Moreover, trafficking of apical GLUT2 is rapidly up-regulated by glucose and artificial sweeteners, which act through T1R2 + T1R3/alpha-gustducin to activate PLC-beta2 and PKC-beta II. Fructose is transported separately by the brush border GLUT5 and then released out of the enterocyte into the blood by GLUT2.
hsa04962	Vasopressin-regulated water reabsorption - Homo sapiens (human)	Organismal Systems; Excretory System	551:AVP|554:AVPR2|2778:GNAS|112:ADCY6|109:ADCY3|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|397:ARHGDIB|396:ARHGDIA|1385:CREB1|10488:CREB3|64764:CREB3L2|84699:CREB3L3|148327:CREB3L4|90993:CREB3L1|9586:CREB5|359:AQP2|8766:RAB11A|9230:RAB11B|1778:DYNC1H1|79659:DYNC2H1|1780:DYNC1I1|1781:DYNC1I2|1783:DYNC1LI2|51143:DYNC1LI1|51626:DYNC2LI1|140735:DYNLL2|8655:DYNLL1|1639:DCTN1|10540:DCTN2|51164:DCTN4|84516:DCTN5|10671:DCTN6|6844:VAMP2|4905:NSF|6810:STX4|5868:RAB5A|5869:RAB5B|5878:RAB5C|361:AQP4|360:AQP3	Congenital nephrogenic diabetes insipidus (NDI)|Asphyxiating thoracic dystrophy|Distal hereditary motor neuropathies (dHMN)	Vasopressin (JP16/USP)|Desmopressin (INN)|Lypressin (USP/INN)|Tolvaptan (JAN/USAN/INN)|Conivaptan hydrochloride (JAN/USAN)|Mozavaptane hydrochloride (JAN)|Desmopressin acetate hydrate (JAN)|Argipressin tannate (USAN)|Lixivaptan (USAN/INN)|Terlipressin (USAN/INN)|Ornipressin (INN)|Conivaptan (INN)	In the kidney, the antidiuretic hormone vasopressin (AVP) is a critical regulator of water homeostasis by controlling the water movement from lumen to the interstitium for water reabsorption and adjusting the urinary water excretion. In normal physiology, AVP is secreted into the circulation by the posterior pituitary gland, in response to an increase in serum osmolality or a decrease in effective circulating volume. When reaching the kidney, AVP binds to V2 receptors on the basolateral surface of the collecting duct epithelium, triggering a G-protein-linked signaling cascade, which leads to water channel aquaporin-2 (AQP2) vesicle insertion into the apical plasma membrane. This results in higher water permeability in the collecting duct and, driven by an osmotic gradient, pro-urinary water then passes the membrane through AQP2 and leaves the cell on the basolateral side via AQP3 and AQP4 water channels, which are constitutively expressed on the basolateral side of these cells. When isotonicity is restored, reduced blood AVP levels results in AQP2 internalization, leaving the apical membrane watertight again.
hsa05412	Arrhythmogenic right ventricular cardiomyopathy (ARVC) - Homo sapiens (human)	Human Diseases; Cardiovascular Diseases	3672:ITGA1|3673:ITGA2|3674:ITGA2B|3675:ITGA3|3676:ITGA4|3678:ITGA5|3655:ITGA6|3679:ITGA7|8516:ITGA8|3680:ITGA9|8515:ITGA10|22801:ITGA11|3685:ITGAV|3688:ITGB1|3690:ITGB3|3691:ITGB4|3693:ITGB5|3694:ITGB6|3695:ITGB7|3696:ITGB8|6444:SGCD|6445:SGCG|6442:SGCA|6443:SGCB|1605:DAG1|1756:DMD|1674:DES|60:ACTB|71:ACTG1|2010:EMD|4000:LMNA|1499:CTNNB1|6932:TCF7|83439:TCF7L1|6934:TCF7L2|51176:LEF1|775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|782:CACNB1|783:CACNB2|784:CACNB3|785:CACNB4|781:CACNA2D1|9254:CACNA2D2|55799:CACNA2D3|93589:CACNA2D4|786:CACNG1|10369:CACNG2|10368:CACNG3|27092:CACNG4|27091:CACNG5|59285:CACNG6|59284:CACNG7|59283:CACNG8|6262:RYR2|1000:CDH2|3728:JUP|1496:CTNNA2|1495:CTNNA1|29119:CTNNA3|81:ACTN4|88:ACTN2|87:ACTN1|89:ACTN3|1824:DSC2|5318:PKP2|1832:DSP|1829:DSG2|2697:GJA1|3908:LAMA2|488:ATP2A2|6546:SLC8A1	Arrhythmogenic right ventricular cardiomyopathy (ARVC)|Naxos disease and Carvajal syndrome|Brugada syndrome (BRS)		Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited heart muscle disease that may result in arrhythmia, heart failure, and sudden death. The hallmark pathological findings are progressive myocyte loss and fibrofatty replacement, with a predilection for the right ventricle. A number of genetic studies have identified mutations in various components of the cardiac desmosome that have important roles in the pathogenesis of ARVC. Disruption of desmosomal function by defective proteins might lead to death of myocytes under mechanical stress. The myocardial injury may be accompanied by inflammation. Since regeneration of cardiac myocytes is limited, repair by fibrofatty replacement occurs. Several studies have implicated that desmosome dysfunction results in the delocalization and nuclear translocation of plakoglobin. As a result, competition between plakoglobin and beta-catenin will lead to the inhibition of Wnt/beta-catenin signaling, resulting in a shift from a myocyte fate towards an adipocyte fate of cells. The ryanodine receptor plays a crucial part in electromechanical coupling by control of release of calcium from the sarcoplasmic reticulum into the cytosol. Therefore, defects in this receptor could result in an imbalance of calcium homeostasis that might trigger cell death.
hsa00620	Pyruvate metabolism - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	55902:ACSS2|84532:ACSS1|5160:PDHA1|5161:PDHA2|5162:PDHB|1737:DLAT|1738:DLD|5315:PKM2|5313:PKLR|31:ACACA|32:ACACB|98:ACYP2|97:ACYP1|219:ALDH1B1|224:ALDH3A2|217:ALDH2|501:ALDH7A1|223:ALDH9A1|134526:ACOT12|92483:LDHAL6B|3948:LDHC|3939:LDHA|160287:LDHAL6A|3945:LDHB|197257:LDHD|2739:GLO1|3029:HAGH|84264:HAGHL|9380:GRHPR|231:AKR1B1|4200:ME2|4199:ME1|10873:ME3|5091:PC|4190:MDH1|4191:MDH2|5106:PCK2|5105:PCK1|38:ACAT1|39:ACAT2|57016:AKR1B10	Pyruvate dehydrogenase complex deficiency|Pyruvate carboxylase deficiency|Pyruvate kinase (PK) deficiency	Cyanamide (JP16)|Disulfiram (JP16/USP/INN)	
hsa00562	Inositol phosphate metabolism - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	5289:PIK3C3|4534:MTM1|5298:PI4KB|5297:PI4KA|55361:PI4K2A|55300:PI4K2B|8394:PIP5K1A|8395:PIP5K1B|23396:PIP5K1C|138429:PIP5KL1|8871:SYNJ2|3633:INPP5B|56623:INPP5E|8867:SYNJ1|4952:OCRL|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|84812:PLCD4|113026:PLCD3|5333:PLCD1|51196:PLCE1|5335:PLCG1|5336:PLCG2|89869:PLCZ1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|5728:PTEN|5305:PIP4K2A|8396:PIP4K2B|79837:PIP4K2C|5288:PIK3C2G|5287:PIK3C2B|5286:PIK3C2A|8821:INPP4B|3631:INPP4A|200576:PIKFYVE|3612:IMPA1|3613:IMPA2|10423:CDIPT|51477:ISYNA1|3628:INPP1|3636:INPPL1|3632:INPP5A|27124:INPP5J|51763:INPP5K|9562:MINPP1|3706:ITPKA|3707:ITPKB|3705:ITPK1|253430:IPMK|64768:IPPK|55586:MIOX|4329:ALDH6A1|7167:TPI1|54928:IMPAD1|3635:INPP5D	Joubert syndrome|Lowe syndrome|Dent disease|Centronuclear myopathy|Lethal congenital contractural syndrome (LCCS)|Fleck corneal dystrophy (FCD)|VACTERL/VATER association		
hsa05166	HTLV-I infection - Homo sapiens (human)	Human Diseases; Infectious Diseases	7040:TGFB1|7042:TGFB2|7043:TGFB3|6513:SLC2A1|8829:NRP1|7412:VCAM1|915:CD3D|916:CD3E|917:CD3G|3383:ICAM1|3683:ITGAL|3689:ITGB2|7094:TLN1|83660:TLN2|4609:MYC|8295:TRRAP|10524:KAT5|894:CCND2|8498:RANBP3|5901:RAN|7514:XPO1|3133:HLA-E|3134:HLA-F|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|811:CALR|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|4776:NFATC4|4772:NFATC1|4773:NFATC2|4775:NFATC3|10725:NFAT5|821:CANX|3560:IL2RB|3561:IL2RG|3716:JAK1|3718:JAK3|6776:STAT5A|6777:STAT5B|2224:FDPS|3265:HRAS|3845:KRAS|4893:NRAS|6237:RRAS|22800:RRAS2|22808:MRAS|7416:VDAC1|292:SLC25A5|293:SLC25A6|291:SLC25A4|83447:SLC25A31|7417:VDAC2|7419:VDAC3|706:TSPO|55697:VAC14|5902:RANBP1|4085:MAD2L1|701:BUB1B|9184:BUB3|991:CDC20|64682:ANAPC1|29882:ANAPC2|996:CDC27|29945:ANAPC4|51433:ANAPC5|8881:CDC16|51434:ANAPC7|8697:CDC23|10393:ANAPC10|51529:ANAPC11|246184:CDC26|10744:PTTG2|9232:PTTG1|1026:CDKN1A|5111:PCNA|5424:POLD1|5425:POLD2|10714:POLD3|57804:POLD4|5426:POLE|5427:POLE2|54107:POLE3|56655:POLE4|595:CCND1|896:CCND3|1019:CDK4|5925:RB1|1871:E2F3|1869:E2F1|1870:E2F2|1029:CDKN2A|1030:CDKN2B|7471:WNT1|7482:WNT2B|7472:WNT2|7473:WNT3|89780:WNT3A|54361:WNT4|7474:WNT5A|81029:WNT5B|7475:WNT6|7477:WNT7B|7476:WNT7A|7479:WNT8B|7478:WNT8A|7483:WNT9A|7484:WNT9B|7480:WNT10B|80326:WNT10A|7481:WNT11|51384:WNT16|8321:FZD1|8324:FZD7|2535:FZD2|7976:FZD3|8322:FZD4|8325:FZD8|7855:FZD5|8323:FZD6|8326:FZD9|11211:FZD10|1856:DVL2|1857:DVL3|1855:DVL1|2932:GSK3B|1499:CTNNB1|10297:APC2|324:APC|1739:DLG1|5154:PDGFA|5155:PDGFB|5156:PDGFRA|5159:PDGFRB|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|207:AKT1|208:AKT2|10000:AKT3|7124:TNF|7132:TNFRSF1A|4214:MAP3K1|6416:MAP2K4|5602:MAPK10|5601:MAPK9|5599:MAPK8|3725:JUN|2874:GPS2|3554:IL1R1|7850:IL1R2|4215:MAP3K3|1147:CHUK|3551:IKBKB|8517:IKBKG|4792:NFKBIA|4790:NFKB1|5970:RELA|4055:LTBR|958:CD40|115650:TNFRSF13C|9020:MAP3K14|5971:RELB|4791:NFKB2|3558:IL2|3559:IL2RA|3600:IL15|3601:IL15RA|3569:IL6|1437:CSF2|4049:LTA|598:BCL2L1|330:BIRC3|331:XIAP|329:BIRC2|7538:ZFP36|4801:NFYB|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|6722:SRF|2005:ELK4|2002:ELK1|6688:SPI1|2114:ETS2|2113:ETS1|387332:TBPL2|9519:TBPL1|6908:TBP|2353:FOS|1958:EGR1|1959:EGR2|8061:FOSL1|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|1385:CREB1|466:ATF1|1386:ATF2|467:ATF3|468:ATF4|7494:XBP1|23373:CRTC1|200186:CRTC2|64784:CRTC3|1387:CREBBP|2033:EP300|8850:KAT2B|2648:KAT2A|6929:TCF3|5423:POLB|1031:CDKN2C|3932:LCK|7015:TERT|4602:MYB|4603:MYBL1|4605:MYBL2|7046:TGFBR1|7048:TGFBR2|4087:SMAD2|4088:SMAD3|4089:SMAD4|472:ATM|545:ATR|1111:CHEK1|11200:CHEK2|7157:TP53|581:BAX|94241:TP53INP1|4488:MSX2|4487:MSX1|112401:BIRC8|79444:BIRC7|9133:CCNB2	Adult T-cell leukemia		Human T-lymphotropic virus type 1 (HTLV-1) is a pathogenic retrovirus that is associated with adult T-cell leukemia/lymphoma (ATL). It is also strongly implicated in non-neoplastic chronic inflammatory diseases such as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Expression of Tax, a viral regulatory protein is critical to the pathogenesis. Tax is a transcriptional co-factor that interfere several signaling pathways related to anti-apoptosis or cell proliferation. The modulation of the signaling by Tax involve its binding to transcription factors like CREB/ATF, NF-kappa B, SRF, and NFAT.
hsa00280	Valine, leucine and isoleucine degradation - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	586:BCAT1|587:BCAT2|259307:IL4I1|593:BCKDHA|594:BCKDHB|1629:DBT|1738:DLD|35:ACADS|34:ACADM|3712:IVD|36:ACADSB|27034:ACAD8|3030:HADHA|1962:EHHADH|1892:ECHS1|3033:HADH|3028:HSD17B10|30:ACAA1|10449:ACAA2|3032:HADHB|5095:PCCA|5096:PCCB|84693:MCEE|4594:MUT|26275:HIBCH|11112:HIBADH|4329:ALDH6A1|219:ALDH1B1|224:ALDH3A2|217:ALDH2|501:ALDH7A1|223:ALDH9A1|316:AOX1|18:ABAT|56922:MCCC1|64087:MCCC2|549:AUH|3155:HMGCL|5019:OXCT1|64064:OXCT2|38:ACAT1|39:ACAT2|3158:HMGCS2|3157:HMGCS1	Maple syrup urine disease (MSUD)|Isovaleric acidemia (IVA)|Methylmalonic aciduria (MMA)|Propionic acidemia|3-Hydroxy-3-methylglutaryl-CoA lyase deficiency|3-Methylcrotonylglycinuria|Mitochondrial respiratory chain deficiencies (MRCD)|Disorders of fatty-acid oxidation|3-Methylglutaconic aciduria (MGCA)|2-Methyl-3-hydroxybutyryl-CoA dehydrogenase (MHBD) deficiency|Alpha-methylacetoacetic aciduria|Succinyl CoA:3-oxoacid CoA transferase (SCOT) deficiency|HMG-CoA synthase (HMGCS) deficiency	Cyanamide (JP16)|Disulfiram (JP16/USP/INN)|Valproic acid (USP)|Vigabatrin (JAN/USAN/INN)|Sodium valproate (JP16)|Calcium valproate	
hsa05120	Epithelial cell signaling in Helicobacter pylori infection - Homo sapiens (human)	Human Diseases; Infectious Diseases	5781:PTPN11|4233:MET|5335:PLCG1|5336:PLCG2|7082:TJP1|50848:F11R|58494:JAM2|83700:JAM3|150084:IGSF5|6868:ADAM17|1839:HBEGF|1956:EGFR|3576:IL8|3577:CXCR1|3579:CXCR2|102:ADAM10|6714:SRC|4067:LYN|1445:CSK|5879:RAC1|998:CDC42|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|5058:PAK1|6416:MAP2K4|5602:MAPK10|5601:MAPK9|5599:MAPK8|3725:JUN|9020:MAP3K14|1147:CHUK|3551:IKBKB|8517:IKBKG|4792:NFKBIA|4790:NFKB1|5970:RELA|10392:NOD1|6352:CCL5|5803:PTPRZ1|28964:GIT1|836:CASP3|523:ATP6V1A|526:ATP6V1B2|525:ATP6V1B1|528:ATP6V1C1|245973:ATP6V1C2|51382:ATP6V1D|529:ATP6V1E1|90423:ATP6V1E2|9296:ATP6V1F|9550:ATP6V1G1|534:ATP6V1G2|127124:ATP6V1G3|8992:ATP6V0E1|155066:ATP6V0E2|535:ATP6V0A1|50617:ATP6V0A4|23545:ATP6V0A2|10312:TCIRG1|9114:ATP6V0D1|245972:ATP6V0D2|51606:ATP6V1H|537:ATP6AP1|527:ATP6V0C|533:ATP6V0B|2919:CXCL1	Helicobacter pylori infection		Two major virulence factors of H. pylori are the vacuolating cytotoxin (VacA) and the cag type-IV secretion system (T4SS) and its translocated effector protein, cytotoxin-associated antigen A (CagA).|VacA binds to lipid rafts and glycosylphosphatidylinositol-anchored proteins (GPI-APs) of the target cell membrane. After insertion into the plasma membrane, VacA channels are endocytosed and eventually reach late endosomal compartments, increasing their permeability to anions with enhancement of the electrogenic vacuolar ATPase (v-ATPase) proton pump. In the presence of weak bases, osmotically active acidotropic ions will accumulate in the endosomes. This leads to water influx and vesicle swelling, an essential step in vacuole formation. In addition, it is reported that the VacA cleavage product binds to the tyrosine phosphatase receptor zeta (Ptprz) on epithelial cells and the induced signaling leads to the phosphorylation of the G protein-coupled receptor kinase-interactor 1 (Git1) and induces ulcerogenesis in mice.|The other virulence factor cag T4SS mediates the translocation of the effector protein CagA, which is subsequently phosphorylated by a Src kinase. Phosphorylated CagA interacts with the protein tyrosine phosphatase SHP-2, thus stimulating its phosphatase activity. Activated SHP-2 is able to induce MAPK signalling through Ras/Raf-dependent and -independent mechanisms. Deregulation of this pathway by CagA may lead to abnormal proliferation and movement of gastric epithelial cells.
hsa04610	Complement and coagulation cascades - Homo sapiens (human)	Organismal Systems; Immune System	2161:F12|3818:KLKB1|3827:KNG1|623:BDKRB1|624:BDKRB2|2160:F11|2158:F9|2157:F8|7450:VWF|2152:F3|2155:F7|2159:F10|2153:F5|2147:F2|2243:FGA|2244:FGB|2266:FGG|2162:F13A1|2165:F13B|7056:THBD|5624:PROC|5627:PROS1|5327:PLAT|5328:PLAU|5340:PLG|7035:TFPI|3053:SERPIND1|1361:CPB2|5054:SERPINE1|5345:SERPINF2|462:SERPINC1|5104:SERPINA5|2:A2M|5265:SERPINA1|2149:F2R|5329:PLAUR|712:C1QA|713:C1QB|714:C1QC|715:C1R|716:C1S|717:C2|720:C4A|721:C4B|718:C3|629:CFB|1675:CFD|4153:MBL2|5648:MASP1|10747:MASP2|727:C5|729:C6|730:C7|731:C8A|732:C8B|733:C8G|735:C9|710:SERPING1|722:C4BPA|725:C4BPB|3075:CFH|3426:CFI|1604:CD55|4179:CD46|966:CD59|719:C3AR1|728:C5AR1|1378:CR1|1380:CR2	Classic complement pathway component defects|Late complement pathway defects|Alternative complement pathway component defects|Mannose-binding lectin pathway component defects|Complement regulatory protein defects|Hemophilia|Factor V deficiency|Afibrinogenemia|Inherited thrombophilia|Familial amyloidosis|Factor XI deficiency|Factor XII deficiency|Factor XIII deficiency|Alpha-2-plasmin inhibitor (a2-PI) deficiency|Hereditary angioedema|Fletcher factor deficiency|Alpha-1-antitrypsin (A1AT) deficiency|Plasminogen activator inhibitor type 1 (PAI-1) deficiency|Plasminogen deficiency	Thrombin (JP16/USP/INN)|Epsilon-Aminocaproic acid (JAN)|Argatroban hydrate (JP16)|Tranexamic acid (JP16/USAN/INN)|Gabexate mesilate (JP16)|Fondaparinux sodium (JAN/USAN/INN)|Ximelagatran (JAN/USAN/INN)|Heparin sodium (JP16/USP/INN)|Anticoagulant heparin (USP)|Aprotinin solution (JAN)|Bivalirudin (USAN/INN)|Apixaban (JAN/USAN/INN)|Reviparin sodium (JAN)|Dalteparin sodium (JAN/USAN/INN)|Danaparoid sodium (JAN/USAN)|Enoxaparin sodium (JAN/USAN/INN)|Desirudin (USAN/INN)|Efegatran sulfate (USAN)|Napsagatran (USAN)|Ecallantide (USAN/INN)|Eculizumab (genetical recombination) (JAN)|Razaxaban hydrochloride (USAN)|Fidexaban (USAN/INN)|Heparin calcium (JP16/USAN)|Icatibant acetate (USAN)|Parnaparin sodium (JP16)|Tinzaparin sodium (USAN)|Lepirudin (INN)|Dabigatran etexilate methanesulfonate (JAN)|Rivaroxaban (JAN/USAN/INN)|Melagatran (INN)|Adomiparin (USAN)|Gabexate (INN)|Betrixaban (USAN)|Eribaxaban (USAN)|Edoxaban tosilate hydrate (JAN)|Edoxaban (USAN/INN)|Darexaban maleate (JAN)	The complement system is a proteolytic cascade in blood plasma and a mediator of innate immunity, a nonspecific defense mechanism against pathogens. There are three pathways of complement activation: the classical pathway, the lectin pathway, and the alternative pathway. All of these pathways generate a crucial enzymatic activity that, in turn, generates the effector molecules of complement. The main consequences of complement activation are the opsonization of pathogens, the recruitment of inflammatory and immunocompetent cells, and the direct killing of pathogens. Blood coagulation is another series of proenzyme-to-serine protease conversions, culminating the formation of thrombin, the enzyme responsible for the conversion of soluble fibrinogen to the insoluble fibrin clot. Protease-activated receptors, such as those activated by thrombin, are members of G protein-coupled receptors and function as a mediator of innate immunity. The kallikrein-kinin system is an endogenous metabolic cascade, triggering of which results in the release of vasoactive kinins (bradykinin-related peptides). Kinin peptides are implicated in many physiological and pathological processes including the regulation of blood pressure and sodium homeostasis, inflammatory processes, and the cardioprotective effects of preconditioning.
hsa00532	Glycosaminoglycan biosynthesis - chondroitin sulfate - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	64132:XYLT2|64131:XYLT1|11285:B4GALT7|126792:B3GALT6|27087:B3GAT1|135152:B3GAT2|26229:B3GAT3|55454:CSGALNACT2|55790:CSGALNACT1|22856:CHSY1|337876:CHSY3|79586:CHPF|54480:CHPF2|50515:CHST11|55501:CHST12|166012:CHST13|9469:CHST3|56548:CHST7|29940:DSE|113189:CHST14|10090:UST|51363:CHST15	SEMD, Omani type|Ehlers-Danlos syndrome (EDS)		Glycosaminoglycans (GAGs) are linear polysaccharide chains consisting of repeating disaccharide units and form proteglycans by covalently attaching to their core proteins. Chondroitin sulfate (CS) is a glycosaminoglycan with the disaccharide unit GalNAc(b1-4)GlcA(b1-3), modified with ester-linked sulfate at certain positions. Dermatan sulfate (DS) is a modified form of CS, in which a portion of D-glucuronate residues is epimerized to L-iduronates. CS and DS are linked to serine residues in core proteins via a linkage tetrasaccharide formed by the transfer of xylose and three more residues [MD:M00057]. The assembly process of CS is initiated by the transfer of N-acetylgalactosamine to the linkage tetrasaccharide. The polymerization step is catalyzed by bifunctional enzymes (chondroitin synthases) that have both b1-3 glucuronosyltransferase and b1-4 N-acetylgalactosaminyltransferase activities [MD:M00058]. Chondroitin polymerization also requires the action of the chondroitin polymerizing factor. Sulfation of chondroitin in vertebrates is a complex process, with multiple sulfotransferases involved in 4-O sulfation and 6-O sulfation of N-acetylgalactosamine residues. Additional enzymes exist for epimerization of glucuronic acid to iduronic acid in DS, sulfation at the C-2 position of the uronic acids, and other patterns of sulfation found in unusual species of chondroitin.
hsa00650	Butanoate metabolism - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	38:ACAT1|39:ACAT2|3033:HADH|3030:HADHA|1962:EHHADH|1892:ECHS1|35:ACADS|341392:ACSM4|6296:ACSM3|348158:ACSM2B|54988:ACSM5|116285:ACSM1|123876:ACSM2A|79944:L2HGDH|7915:ALDH5A1|18:ABAT|2571:GAD1|2572:GAD2|3158:HMGCS2|3157:HMGCS1|3155:HMGCL|5019:OXCT1|64064:OXCT2|65985:AACS|622:BDH1|56898:BDH2|5160:PDHA1|5161:PDHA2|5162:PDHB	3-Hydroxy-3-methylglutaryl-CoA lyase deficiency|Succinic semialdehyde dehydrogenase (SSADH) deficiency|Cerebral palsy|Succinyl CoA:3-oxoacid CoA transferase (SCOT) deficiency|HMG-CoA synthase (HMGCS) deficiency	Valproic acid (USP)|Vigabatrin (JAN/USAN/INN)|Sodium valproate (JP16)|Calcium valproate	
hsa04744	Phototransduction - Homo sapiens (human)	Organismal Systems; Sensory System	6010:RHO|6011:GRK1|131890:GRK7|5957:RCVRN|409:ARRB2|408:ARRB1|346562:GNAT3|2780:GNAT2|2779:GNAT1|2782:GNB1|2792:GNGT1|8787:RGS9|5145:PDE6A|5158:PDE6B|5148:PDE6G|3000:GUCY2D|2986:GUCY2F|2979:GUCA1B|2978:GUCA1A|9626:GUCA1C|9187:SLC24A1|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|1259:CNGA1|1258:CNGB1	Cone-rod dystrophy and cone dystrophy|Retinitis pigmentosa (RP)|Congenital stationary night blindness (CSNB)|Familial flecked retina syndrome|Leber congenital amaurosis (LCR)|Bradyopsia		Phototransduction is a biochemical process by which the photoreceptor cells generate electrical signals in response to captured photons. The vertebrate cascade starts with the absorption of photons by the photoreceptive pigments, the rhodopsins, which consist of a membrane embedded chromophore, 11-cis-retinal, and a G-protein-coupled receptor, opsin. The photon isomerizes 11-cis-retinal to all-trans-retinal which induces a structural change that activates the opsin. This triggers hydrolysis of cGMP by activating a transducinphosphodiesterase 6 (PDE6) cascade, which results in closure of the cGMP-gated cation channels (CNG) in the plasma membrane and membrane hyperpolarization. The hyperpolarization of the membrane potential of the photoreceptor cell modulates the release of neurotransmitters to downstream cells. Recovery from light involves the deactivation of the light- activated intermediates: photolyzed rhodopsin is phosphorylated by rhodopsin kinase (RK) and subsequently capped off by arrestin; GTP-binding transducin alpha subunit deactivates through a process that is stimulated by RGS9.
hsa00534	Glycosaminoglycan biosynthesis - heparan sulfate - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	64132:XYLT2|64131:XYLT1|11285:B4GALT7|126792:B3GALT6|27087:B3GAT1|135152:B3GAT2|26229:B3GAT3|2135:EXTL2|2137:EXTL3|2134:EXTL1|2131:EXT1|2132:EXT2|3340:NDST1|8509:NDST2|9348:NDST3|64579:NDST4|26035:GLCE|9653:HS2ST1|9394:HS6ST1|90161:HS6ST2|266722:HS6ST3|9957:HS3ST1|9956:HS3ST2|9955:HS3ST3A1|9953:HS3ST3B1|222537:HS3ST5	Multiple exostoses|Ehlers-Danlos syndrome (EDS)		Heparan sulfate (HS) is a glycosaminoglycan with the basic disaccharide unit GlcNAc(a1-4)GlcA(b1-4), containing N- and O-sulfate esters at various positions. HS is covalently attached to serine residues in a proteoglycan core protein via the linkage tetrasaccharide. The addition of the first GlcNAc residue is catalyzed by EXTL3 glycosyltransferase, followed by the polymerization steps catalyzed by EXT1 and EXT2 transferases. As the chains polymerize, HS undergoes a series of modification reactions catalyzed by at least four families of sulfotransferases and one epimerase.
hsa04723	Retrograde endocannabinoid signaling - Homo sapiens (human)	Organismal Systems; Nervous System	57084:SLC17A6|57030:SLC17A7|246213:SLC17A8|2890:GRIA1|2891:GRIA2|2892:GRIA3|2893:GRIA4|775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|2911:GRM1|2915:GRM5|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|3708:ITPR1|3709:ITPR2|3710:ITPR3|222236:NAPEPLD|5579:PRKCB|5578:PRKCA|5582:PRKCG|747:DAGLA|5743:PTGS2|57406:ABHD6|2166:FAAH|1268:CNR1|2773:GNAI3|2770:GNAI1|2771:GNAI2|2775:GNAO1|2782:GNB1|2783:GNB2|2784:GNB3|59345:GNB4|10681:GNB5|54331:GNG2|2785:GNG3|2786:GNG4|2787:GNG5|2788:GNG7|94235:GNG8|2790:GNG10|2791:GNG11|55970:GNG12|51764:GNG13|2792:GNGT1|2793:GNGT2|3760:KCNJ3|3763:KCNJ6|3765:KCNJ9|3762:KCNJ5|773:CACNA1A|774:CACNA1B|5594:MAPK1|5595:MAPK3|5602:MAPK10|5601:MAPK9|5599:MAPK8|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|11343:MGLL|140679:SLC32A1|22999:RIMS1|2555:GABRA2|2554:GABRA1|2557:GABRA4|2556:GABRA3|2558:GABRA5|2559:GABRA6|2560:GABRB1|2562:GABRB3|2561:GABRB2|2566:GABRG2|2565:GABRG1|2567:GABRG3|2563:GABRD|2564:GABRE|55879:GABRQ|2568:GABRP|221955:DAGLB|200959:GABRR3|2569:GABRR1|2570:GABRR2	Syndromic X-linked mental retardation with epilepsy or seizures		Endogenous cannabinoids (endocannabinoids) serve as retrograde messengers at synapses in various regions of the brain. The family of endocannabinoids includes at least five derivatives of arachidonic acid; the two best characterized are arachydonoyl ethanolamide (anandamide, AEA) and 2-arachydonoil glycerol (2AG). They are released from postsynaptic neurons upon postsynaptic depolarization and/or receptor activation. The released endocannabinoids then activate the CB1 receptors (CB1R) at presynaptic terminals and suppress the release of inhibitory transmitter GABA (depolarization-induced suppression of inhibition, DSI) or excitatory transmitter glutamate (depolarization-induced suppression of excitation, DSE) by inhibiting Ca2+ channels. Whereas DSI and DSE result in short-term synaptic plasticity, endocannabinoids also mediate long-term synaptic changes (eCB-LTD). Persistent activation of CB1 receptors over a period of minutes triggers eCB-LTD by a RIM1alpha-dependent mechanism.
hsa04012	ErbB signaling pathway - Homo sapiens (human)	Environmental Information Processing; Signal Transduction	1950:EGF|7039:TGFA|374:AREG|1956:EGFR|2064:ERBB2|5335:PLCG1|5336:PLCG2|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|5579:PRKCB|5578:PRKCA|5582:PRKCG|23624:CBLC|868:CBLB|867:CBL|6714:SRC|5747:PTK2|1399:CRKL|1398:CRK|25:ABL1|27:ABL2|8440:NCK2|4690:NCK1|5058:PAK1|5062:PAK2|5063:PAK3|10298:PAK4|56924:PAK6|57144:PAK7|6416:MAP2K4|5609:MAP2K7|5602:MAPK10|5601:MAPK9|5599:MAPK8|3725:JUN|2002:ELK1|685:BTC|1839:HBEGF|2069:EREG|2065:ERBB3|3084:NRG1|9542:NRG2|2066:ERBB4|25759:SHC2|6464:SHC1|53358:SHC3|399694:SHC4|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|4609:MYC|2549:GAB1|10718:NRG3|145957:NRG4|6776:STAT5A|6777:STAT5B|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|2475:MTOR|6199:RPS6KB2|6198:RPS6KB1|1978:EIF4EBP1|572:BAD|2932:GSK3B|1026:CDKN1A|1027:CDKN1B	PTEN hamartoma tumor syndrome (PHTS)|Lethal congenital contractural syndrome (LCCS)|Growth hormone insensitivity with immunodeficiency|Pituitary adenomas	Gefitinib (JAN/USAN/INN)|Bosutinib (USAN)|Trastuzumab (genetical recombination) (JAN)|Canertinib dihydrochloride (USAN)|Cetuximab (genetical recombination) (JAN)|Dasatinib (INN)|Erlotinib hydrochloride (JAN/USAN)|Lapatinib tosilate hydrate (JAN)|Mubritinib (USAN/INN)|Panitumumab (genetical recombination) (JAN)|Pelitinib (USAN/INN)|Pertuzumab (genetical recombination) (JAN)|Temsirolimus (JAN/USAN/INN)|Sorafenib tosilate (JAN)|Vandetanib (JAN/USAN/INN)|Nilotinib hydrochloride hydrate (JAN)|Dasatinib hydrate (JAN)|Erlotinib (INN)|Lapatinib (INN)|Sorafenib (USAN/INN)|Neratinib (INN/USAN)|Nilotinib (USAN/INN)|Afatinib (USAN/INN)|Bosutinib hydrate (JAN)|Afatinib maleate (JAN)|Zalutumumab (USAN/INN)	The ErbB family of receptor tyrosine kinases (RTKs) couples binding of extracellular growth factor ligands to intracellular signaling pathways regulating diverse biologic responses, including proliferation, differentiation, cell motility, and survival. Ligand binding to the four closely related members of this RTK family -epidermal growth factor receptor (EGFR, also known as ErbB-1 or HER1), ErbB-2 (HER2), ErbB-3 (HER3), and ErbB-4 (HER4)-induces the formation of receptor homo- and heterodimers and the activation of the intrinsic kinase domain, resulting in phosphorylation on specific tyrosine residues (pY) within the cytoplasmic tail. Signaling effectors containing binding pockets for pY-containing peptides are recruited to activated receptors and induce the various signaling pathways. The Shc- and/or Grb2-activated mitogen-activated protein kinase (MAPK) pathway is a common target downstream of all ErbB receptors. Similarly, the phosphatidylinositol-3-kinase (PI-3K) pathway is directly or indirectly activated by most ErbBs. Several cytoplasmic docking proteins appear to be recruited by specific ErbB receptors and less exploited by others. These include the adaptors Crk, Nck, the phospholipase C gamma (PLCgamma), the intracellular tyrosine kinase Src, or the Cbl E3 ubiquitin protein ligase.
hsa00330	Arginine and proline metabolism - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	2628:GATM|2593:GAMT|1159:CKMT1B|1152:CKB|1160:CKMT2|1158:CKM|548596:CKMT1A|113451:ADC|79814:AGMAT|4953:ODC1|6723:SRM|6611:SMS|262:AMD1|26:ABP1|219:ALDH1B1|224:ALDH3A2|217:ALDH2|501:ALDH7A1|223:ALDH9A1|84735:CNDP1|55748:CNDP2|57571:CARNS1|112483:SAT2|6303:SAT1|4129:MAOB|4128:MAOA|4942:OAT|5831:PYCR1|29920:PYCR2|65263:PYCRL|5625:PRODH|8659:ALDH4A1|5832:ALDH18A1|51056:LAP3|8974:P4HA2|5033:P4HA1|283208:P4HA3|58510:PRODH2|2805:GOT1|2806:GOT2|1610:DAO|5009:OTC|445:ASS1|435:ASL|383:ARG1|384:ARG2|4842:NOS1|4843:NOS2|4846:NOS3|2744:GLS|27165:GLS2|2752:GLUL|2746:GLUD1|2747:GLUD2|1373:CPS1|162417:NAGS|95:ACY1	Carbamoyl phosphate synthetase I deficiency|Citrullinemia (CTLN)|Hyperargininemia|Ornithine transcarbamylase deficiency|Ornithinaemia|Hyperprolinemia (HP)|Snyder-Robinson syndrome|Guanidinoacetate methyltransferase (GAMT) deficiency|Creatine deficiency syndrome|Congenital systemic glutamine deficiency (CSGD)|Argininosuccinic aciduria (ARGINSA)|N-acetylglutamate synthase (NAGS) deficiency|Aminoacylase 1 deficiency	Cyanamide (JP16)|Disulfiram (JP16/USP/INN)|Isoniazid (JP16/USP/INN)|Phenelzine sulfate (USP)|Selegiline hydrochloride (JAN/USP)|Tranylcypromine sulfate (USP XXI)|Lazabemide hydrochloride (JAN/USAN)|Amezinium metilsulfate (JAN)|Isoniazid calcium pyruvinate (JAN)|Safrazine hydrochloride (JAN)|Isoniazid sodium methanesulfonate hydrate (JAN)|Toloxatone (INN)|Brofaromine (INN)|Moclobemide (USAN/INN)|Rasagiline mesylate (USAN)|Befloxatone (INN)|Pargyline hydrochloride (USAN)|Iproniazid (INN)|Isocarboxazid (INN)|Cimoxatone (INN)|Ladostigil tartrate (USAN)|Clorgiline (INN)|Caroxazone (USAN/INN)|Selegiline (USAN/INN)|Mofegiline hydrochloride (USAN)|Lazabemide (USAN/INN)|Milacemide hydrochloride (USAN)|Nialamide (INN)|Iproclozide (INN)|Iproniazid phosphate|Phenelzine (BAN)|Pargyline (INN)|Rasagiline (USAN/INN)|Tranylcypromine (INN)	
hsa04350	TGF-beta signaling pathway - Homo sapiens (human)	Environmental Information Processing; Signal Transduction	8646:CHRD|9241:NOG|1311:COMP|7059:THBS3|7058:THBS2|7060:THBS4|7057:THBS1|1634:DCN|10468:FST|650:BMP2|652:BMP4|653:BMP5|656:BMP8B|655:BMP7|654:BMP6|353500:BMP8A|151449:GDF7|392255:GDF6|8200:GDF5|268:AMH|7040:TGFB1|7042:TGFB2|7043:TGFB3|4838:NODAL|3625:INHBB|3626:INHBC|83729:INHBE|3624:INHBA|7044:LEFTY2|10637:LEFTY1|92:ACVR2A|93:ACVR2B|659:BMPR2|7048:TGFBR2|269:AMHR2|657:BMPR1A|658:BMPR1B|7046:TGFBR1|90:ACVR1|4090:SMAD5|4093:SMAD9|4086:SMAD1|4087:SMAD2|4088:SMAD3|4089:SMAD4|4091:SMAD6|4092:SMAD7|57154:SMURF1|64750:SMURF2|9765:ZFYVE16|9372:ZFYVE9|3397:ID1|3398:ID2|3399:ID3|3400:ID4|5934:RBL2|5933:RBL1|1874:E2F4|1875:E2F5|7027:TFDP1|1387:CREBBP|2033:EP300|6667:SP1|4609:MYC|1030:CDKN2B|5308:PITX2|9978:RBX1|8454:CUL1|6500:SKP1|5594:MAPK1|5595:MAPK3|3458:IFNG|7124:TNF|387:RHOA|6093:ROCK1|9475:ROCK2|6199:RPS6KB2|6198:RPS6KB1|5518:PPP2R1A|5519:PPP2R1B|5516:PPP2CB|5515:PPP2CA|130399:ACVR1C|4052:LTBP1	Fibrodysplasia ossificans progressiva (FOP)|Ossification of the posterior longitudinal ligament of spine (OPLL)|Camurati-Engelmann disease|Grebe dysplasia|Fibular hypoplasia and complex brachydactyly|Acromesomelic dysplasia with genital anomalies|Brachydactyly|Brachydactyly|Other brachydactylies|Hereditary hemorrhagic telangiectasia (HHT)|46,XY disorders of sex development (Other)|Axenfeld-Rieger syndrome (ARS)|Heterotaxy|Tarsal-carpal coalition syndrome|Loeys-Dietz syndrome (LDS)|Familial thoracic aortic aneurysm and dissection (TAAD)|Klippel-Feil syndrome(KFS)|Stapes ankylosis with broad thumb and toes|Congenital stromal corneal dystrophy (CSCD)|Juvenile polyposis syndrome|Hereditary mixed polyposis syndrome|Anophthalmia and microphthalmia (A/M)|Peters anomaly|Ring dermoid of cornea	Etanercept (genetical recombination) (JAN)|Adalimumab (genetical recombination) (JAN)|Infliximab (genetical recombination) (JAN)|Certolizumab pegol (genetical recombination) (JAN)|Golimumab (genetical recombination) (JAN)	The transforming growth factor-beta (TGF-beta) family members, which include TGF-betas, activins and bone morphogenetic proteins (BMPs), are structurally related secreted cytokines found in species ranging from worms and insects to mammals. A wide spectrum of cellular functions such as proliferation, apoptosis, differentiation and migration are regulated by TGF-beta family members. TGF-beta family member binds to the Type II receptor and recruits Type I, whereby Type II receptor phosphorylates and activates Type I. The Type I receptor, in turn, phosphorylates receptor-activated Smads ( R-Smads: Smad1, Smad2, Smad3, Smad5, and Smad8). Once phosphorylated, R-Smads associate with the co-mediator Smad, Smad4, and the heteromeric complex then translocates into the nucleus. In the nucleus, Smad complexes activate specific genes through cooperative interactions with other DNA-binding and coactivator (or co-repressor) proteins.
hsa00020	Citrate cycle (TCA cycle) - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	1431:CS|47:ACLY|50:ACO2|48:ACO1|3418:IDH2|3417:IDH1|3421:IDH3G|3420:IDH3B|3419:IDH3A|55753:OGDHL|4967:OGDH|1743:DLST|1738:DLD|8802:SUCLG1|8801:SUCLG2|8803:SUCLA2|6389:SDHA|6390:SDHB|6391:SDHC|6392:SDHD|2271:FH|4190:MDH1|4191:MDH2|5091:PC|5106:PCK2|5105:PCK1|5160:PDHA1|5161:PDHA2|5162:PDHB|1737:DLAT	Pyruvate carboxylase deficiency|Mitochondrial DNA depletion syndrome (MDS)|Multiple cutaneous and uterine leiomyomata|Diseases of the tricarboxylic acid cycle		The citrate cycle (TCA cycle, Krebs cycle) is an important aerobic pathway for the final steps of the oxidation of carbohydrates and fatty acids. The cycle starts with acetyl-CoA, the activated form of acetate, derived from glycolysis and pyruvate oxidation for carbohydrates and from beta oxidation of fatty acids. The two-carbon acetyl group in acetyl-CoA is transferred to the four-carbon compound of oxaloacetate to form the six-carbon compound of citrate. In a series of reactions two carbons in citrate are oxidized to CO2 and the reaction pathway supplies NADH for use in the oxidative phosphorylation and other metabolic processes. The pathway also supplies important precursor metabolites including 2-oxoglutarate. At the end of the cycle the remaining four-carbon part is transformed back to oxaloacetate. According to the genome sequence data, many organisms seem to lack genes for the full cycle [MD:M00009], but contain genes for specific segments [MD:M00010 M00011].
hsa04142	Lysosome - Homo sapiens (human)	Cellular Processes; Transport and Catabolism	535:ATP6V0A1|50617:ATP6V0A4|23545:ATP6V0A2|10312:TCIRG1|9114:ATP6V0D1|245972:ATP6V0D2|51606:ATP6V1H|537:ATP6AP1|527:ATP6V0C|533:ATP6V0B|5476:CTSA|1508:CTSB|1075:CTSC|1509:CTSD|1510:CTSE|8722:CTSF|1511:CTSG|1512:CTSH|1513:CTSK|1514:CTSL1|1519:CTSO|1520:CTSS|1515:CTSL2|1521:CTSW|1522:CTSZ|9476:NAPSA|5641:LGMN|1200:TPP1|2717:GLA|2720:GLB1|2548:GAA|2629:GBA|3425:IDUA|4668:NAGA|4669:NAGLU|2581:GALC|2990:GUSB|3073:HEXA|3074:HEXB|4126:MANBA|4125:MAN2B1|4758:NEU1|410:ARSA|411:ARSB|22901:ARSG|2588:GALNS|2799:GNS|3423:IDS|6448:SGSH|3988:LIPA|23659:PLA2G15|1777:DNASE2|58511:DNASE2B|6609:SMPD1|427:ASAH1|175:AGA|5660:PSAP|768239:PSAPL1|2760:GM2A|9374:PPT2|5538:PPT1|3920:LAMP2|3916:LAMP1|27074:LAMP3|968:CD68|967:CD63|950:SCARB2|4864:NPC1|10577:NPC2|1497:CTNS|26503:SLC17A5|4891:SLC11A2|6556:SLC11A1|9741:LAPTM4A|7805:LAPTM5|55353:LAPTM4B|20:ABCA2|23457:ABCB9|8763:CD164|9583:ENTPD4|6272:SORT1|1201:CLN3|1203:CLN5|256471:MFSD8|138050:HGSNAT|285362:SUMF1|79158:GNPTAB|84572:GNPTG|51172:NAGPA|3482:IGF2R|4074:M6PR|1211:CLTA|1212:CLTB|8218:CLTCL1|1213:CLTC|164:AP1G1|162:AP1B1|10053:AP1M2|8907:AP1M1|1174:AP1S1|8905:AP1S2|130340:AP1S3|8943:AP3D1|8120:AP3B2|8546:AP3B1|10947:AP3M2|26985:AP3M1|1176:AP3S1|10239:AP3S2|23431:AP4E1|10717:AP4B1|9179:AP4M1|11154:AP4S1|23163:GGA3|26088:GGA1|23062:GGA2|57192:MCOLN1|2517:FUCA1|3373:HYAL1|53:ACP2|54:ACP5	Glycogen storage diseases (GSD)|Mucopolysaccharidosis type IV (MPS4)|GM2 gangliosidoses|Fabry disease|Gaucher disease|Metachromatic leukodystrophy (MLD)|Mucopolysaccharidosis type I (MPS1)|Mucopolysaccharidosis type II (MPS2)|Mucopolysaccharidosis type III (MPS3)|Mucopolysaccharidosis type VI (MPS6)|Mucopolysaccharidosis type VII (MPS7)|Mucopolysaccharidosis type IX (MPS9)|Krabbe disease|Niemann-Pick type C disease (NPC)|Niemann-Pick disease (NPD), including;|Farber lipogranulomatosis|alpha-Mannosidosis|beta-Mannosidosis|Fucosidosis|Sialidosis|Mucolipidosis II and III|Mucolipidosis IV|Aspartylglucosaminuria (AGU)|Alpha-N-acetylgalactosaminidase deficiency|Sialuria/ Sialic acid storage disease|Lysosomal acid lipase deficiency|Neuronal ceroid lipofuscinosis|Danon disease|Hermansky-Pudlak syndrome (HPS)|Multiple sulfatase deficiency (MSD)|Pycnodysostosis|Papillon-Lefevre syndrome|Cystinosis|Galactosialidosis|GM1 gangliosidosis|Haim-Munk syndrome|Progressive myoclonic epilepsy (PME)|Tropical calcific pancreatitis|Cerebral palsy|Acid phosphatase deficiency|Hypochromic microcytic anemia	Relacatib (USAN/INN)	Lysosomes are membrane-delimited organelles in animal cells serving as the cell's main digestive compartment to which all sorts of macromolecules are delivered for degradation. They contain more than 40 hydrolases in an acidic environment (pH of about 5). After synthesis in the ER, lysosomal enzymes are decorated with mannose-6-phosphate residues, which are recognized by mannose-6-phosphate receptors in the trans-Golgi network. They are packaged into clathrin-coated vesicles and are transported to late endosomes. Substances for digestion are acquired by the lysosomes via a series of processes including endocytosis, phagocytosis, and autophagy.
hsa00472	D-Arginine and D-ornithine metabolism - Homo sapiens (human)	Metabolism; Metabolism of Other Amino Acids	1610:DAO			
hsa00520	Amino sugar and nucleotide sugar metabolism - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	1116:CHI3L1|27159:CHIA|1118:CHIT1|3073:HEXA|3074:HEXB|55577:NAGK|5238:PGM3|6675:UAP1|91373:UAP1L1|10020:GNE|5973:RENBP|54187:NANS|140838:NANP|80896:NPL|55907:CMAS|51700:CYB5R2|51706:CYB5R1|1727:CYB5R3|3101:HK3|3099:HK2|3098:HK1|80201:HKDC1|51005:AMDHD2|64841:GNPNAT1|10007:GNPDA1|132789:GNPDA2|9945:GFPT2|2673:GFPT1|80146:UXS1|2645:GCK|2821:GPI|5236:PGM1|55276:PGM2|7360:UGP2|2592:GALT|7358:UGDH|2585:GALK2|2584:GALK1|2582:GALE|5373:PMM2|5372:PMM1|29925:GMPPB|29926:GMPPA|2762:GMDS|4351:MPI|197258:FUK|8790:FPGT|7264:TSTA3	Galactosemia|Sialuria/ Sialic acid storage disease|Methemoglobinemia|Distal muscular dystrophies|Nonaka distal myopathy (NM)		
hsa04512	ECM-receptor interaction - Homo sapiens (human)	Environmental Information Processing; Signaling Molecules and Interaction	1280:COL2A1|1302:COL11A2|1301:COL11A1|1277:COL1A1|1289:COL5A1|50509:COL5A3|1281:COL3A1|1290:COL5A2|1278:COL1A2|1284:COL4A2|1286:COL4A4|1288:COL4A6|1287:COL4A5|1282:COL4A1|1292:COL6A2|1291:COL6A1|1293:COL6A3|131873:COL6A6|284217:LAMA1|3908:LAMA2|3911:LAMA5|3909:LAMA3|3910:LAMA4|3912:LAMB1|3913:LAMB2|3914:LAMB3|22798:LAMB4|3915:LAMC1|3918:LAMC2|10319:LAMC3|1101:CHAD|5649:RELN|1311:COMP|7059:THBS3|7058:THBS2|7060:THBS4|7057:THBS1|2335:FN1|6696:SPP1|7448:VTN|63923:TNN|7143:TNR|7148:TNXB|3371:TNC|7450:VWF|3381:IBSP|375790:AGRN|3339:HSPG2|3672:ITGA1|3673:ITGA2|3674:ITGA2B|3675:ITGA3|3676:ITGA4|3678:ITGA5|3655:ITGA6|3679:ITGA7|8516:ITGA8|3680:ITGA9|8515:ITGA10|22801:ITGA11|3685:ITGAV|3688:ITGB1|3690:ITGB3|3691:ITGB4|3693:ITGB5|3694:ITGB6|3695:ITGB7|3696:ITGB8|960:CD44|9672:SDC3|6382:SDC1|6385:SDC4|6383:SDC2|9900:SV2A|22987:SV2C|9899:SV2B|948:CD36|2814:GP5|2811:GP1BA|2812:GP1BB|2815:GP9|51206:GP6|1605:DAG1|961:CD47|3161:HMMR	Hemophilia|Bernard-Soulier syndrome|Glanzmann thrombasthenia|Pierson syndrome|Hereditary angiopathy with nephropathy, aneurysms, and muscle cramps (HANAC)|Alport syndrome|Benign familial hematuria|Epidermolysis bullosa, hemidesmosomal|Epidermolysis bullosa, junctional|Congenital myasthenic syndrome|Ehlers-Danlos syndrome (EDS)|Vitreoretinal degeneration|Laryngoonychocutaneous syndrome|Porencephaly|Brain small vessel disease with Axenfeld-Rieger anomaly	Levetiracetam (JAN/USAN/INN)|Tirofiban hydrochloride (USAN)|Abciximab (genetical recombination) (JAN)|Cilengitide (USAN/INN)|Eptifibatide (INN)|Tirofiban (INN)|Valategrast hydrochloride (USAN)	The extracellular matrix (ECM) consists of a complex mixture of structural and functional macromolecules and serves an important role in tissue and organ morphogenesis and in the maintenance of cell and tissue structure and function. Specific interactions between cells and the ECM are mediated by transmembrane molecules, mainly integrins and perhaps also proteoglycans, CD36, or other cell-surface-associated components. These interactions lead to a direct or indirect control of cellular activities such as adhesion, migration, differentiation, proliferation, and apoptosis. In addition, integrins function as mechanoreceptors and provide a force-transmitting physical link between the ECM and the cytoskeleton. Integrins are a family of glycosylated, heterodimeric transmembrane adhesion receptors that consist of noncovalently bound alpha- and beta-subunits.
hsa00785	Lipoic acid metabolism - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	11019:LIAS|387787:LIPT2|51601:LIPT1			
hsa05012	Parkinson's disease - Homo sapiens (human)	Human Diseases; Neurodegenerative Diseases	7317:UBA1|7318:UBA7|7314:UBB|7332:UBE2L3|9246:UBE2L6|118424:UBE2J2|51465:UBE2J1|7327:UBE2G2|7326:UBE2G1|5071:PARK2|6622:SNCA|2861:GPR37|5413:SEPT5|9627:SNCAIP|7345:UCHL1|7054:TH|6531:SLC6A3|6571:SLC18A2|6570:SLC18A1|4535:ND1|4536:ND2|4537:ND3|4538:ND4|4539:ND4L|4540:ND5|4541:ND6|4723:NDUFV1|4729:NDUFV2|4731:NDUFV3|4694:NDUFA1|4695:NDUFA2|4696:NDUFA3|4697:NDUFA4|56901:NDUFA4L2|4698:NDUFA5|4700:NDUFA6|4701:NDUFA7|4702:NDUFA8|4704:NDUFA9|4705:NDUFA10|4706:NDUFAB1|126328:NDUFA11|55967:NDUFA12|51079:NDUFA13|4707:NDUFB1|4708:NDUFB2|4709:NDUFB3|4710:NDUFB4|4711:NDUFB5|4712:NDUFB6|4713:NDUFB7|4714:NDUFB8|4715:NDUFB9|4716:NDUFB10|54539:NDUFB11|4719:NDUFS1|4720:NDUFS2|4722:NDUFS3|4724:NDUFS4|4725:NDUFS5|4726:NDUFS6|374291:NDUFS7|4728:NDUFS8|4717:NDUFC1|4718:NDUFC2|6389:SDHA|6390:SDHB|6391:SDHC|6392:SDHD|7386:UQCRFS1|4519:CYTB|1537:CYC1|7384:UQCRC1|7385:UQCRC2|7388:UQCRH|440567:UQCRHL|7381:UQCRB|27089:UQCRQ|29796:UQCR10|10975:UQCR11|4514:COX3|4512:COX1|4513:COX2|1327:COX4I1|84701:COX4I2|9377:COX5A|1329:COX5B|1337:COX6A1|1339:COX6A2|1340:COX6B1|125965:COX6B2|1345:COX6C|1347:COX7A2|1346:COX7A1|9167:COX7A2L|1349:COX7B|170712:COX7B2|1350:COX7C|1351:COX8A|341947:COX8C|498:ATP5A1|506:ATP5B|509:ATP5C1|513:ATP5D|514:ATP5E|4508:ATP6|515:ATP5F1|518:ATP5G3|516:ATP5G1|517:ATP5G2|10476:ATP5H|539:ATP5O|522:ATP5J|4509:ATP8|120892:LRRK2|65018:PINK1|11315:PARK7|27429:HTRA2|7416:VDAC1|7417:VDAC2|7419:VDAC3|292:SLC25A5|293:SLC25A6|291:SLC25A4|83447:SLC25A31|54205:CYCS|317:APAF1|842:CASP9|836:CASP3|100532726:NDUFC2-KCTD14|10105:PPIF	Parkinson's disease (PD)|Mitochondrial respiratory chain deficiencies (MRCD)|Primary torsion dystonia (PTD)		Parkinson's disease (PD) is a progressive neurodegenerative movement disorder that results primarily from the death of dopaminergic neurons in the substantia nigra. Mutations in alpha-synuclein, UCHL1 (a ubiquitin carboxy-terminal hydrolase L1), parkin, DJ1 (a parkin-associated protein involved with oxidative stress), and PINK1 (a putative serine threonine kinase) are known to cause early-onset PD. These pathogenic mutations are associated with disease through pathogenic pathways that may commonly lead proteasome dysfunction, mitochondrial impairment, and oxidative stress. Point mutations in alpha-synuclein lead to excessive intracellular accumulation and protofibril formation. Decrease in the amount of soluble alpha-synuclein tends to increase free cytoplasmic dopamine and the formation of reactive oxygen species (ROS). Modification of parkin and UCHL1 are associated with the ubiquitin-proteasome system pathway and may increase proteotoxic stress. Mutations in parkin, DJ1, and PINK1 may alter mitochondiral activity, potentially impairing proteasomal function. Environmental toxins such as N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone can cause mitochondrial dysfunction and oxidative stress.
hsa05033	Nicotine addiction - Homo sapiens (human)	Human Diseases; Substance Dependence	1137:CHRNA4|1139:CHRNA7|1141:CHRNB2|116443:GRIN3A|116444:GRIN3B|140679:SLC32A1|200959:GABRR3|246213:SLC17A8|2554:GABRA1|2555:GABRA2|2556:GABRA3|2557:GABRA4|2558:GABRA5|2559:GABRA6|2560:GABRB1|2561:GABRB2|2562:GABRB3|2563:GABRD|2564:GABRE|2565:GABRG1|2566:GABRG2|2567:GABRG3|2568:GABRP|2569:GABRR1|2570:GABRR2|2890:GRIA1|2891:GRIA2|2892:GRIA3|2893:GRIA4|2902:GRIN1|2903:GRIN2A|2904:GRIN2B|2905:GRIN2C|2906:GRIN2D|55879:GABRQ|57030:SLC17A7|57084:SLC17A6|773:CACNA1A|774:CACNA1B|8973:CHRNA6			Nicotine is one of the main psychoactive ingredients in tobacco that contributes to the harmful tobacco smoking habit. A common feature of addictive drugs, including nicotine, is that they increase dopamine (DA) release in the nucleus accumbens (NAc). The principal dopaminergic projections to NAc arise from neurons in the ventral tegmental area (VTA). In the VTA, alpha6- and alpha4beta2-containing nAChRs (alpha6*-AChRs and alpha4beta2*-AChRs, respectively) are located on GABAergic terminals and provide inhibitory inputs onto DAergic neuons, while alpha7*-nAChRs are located on glutamatergic terminals and activation of these receptors enhances glutamate release and increases excitability of DAergic neurons. Nicotine acts as an agonist to activate and desensitize these nicotinic acetylcholine receptors (nAChRs). After a short exposure to nicotine, alpha6*- and alpha4beta2*- nAChRs on GABAergic afferents are desensitized, decreasing GABA release and decreasing local inhibition of DA neurons. But the alpha7*-nAChRs on glutamatergic afferents remain active and enhance glutamate excitation of the DA neurons, leading to increased DA release in the NAc -and so facilitate the reinforcing effects of nicotine.
hsa04978	Mineral absorption - Homo sapiens (human)	Organismal Systems; Digestive System	7421:VDR|140803:TRPM6|54822:TRPM7|55503:TRPV6|795:S100G|1811:SLC26A3|65010:SLC26A6|115019:SLC26A9|1181:CLCN2|6550:SLC9A3|6523:SLC5A1|340024:SLC6A19|476:ATP1A1|480:ATP1A4|478:ATP1A3|477:ATP1A2|481:ATP1B1|482:ATP1B2|483:ATP1B3|23439:ATP1B4|486:FXYD2|3162:HMOX1|3163:HMOX2|79901:CYBRD1|4891:SLC11A2|6556:SLC11A1|94033:FTMT|2495:FTH1|2512:FTL|30061:SLC40A1|9843:HEPH|7018:TF|55630:SLC39A4|7779:SLC30A1|1317:SLC31A1|26872:STEAP1|261729:STEAP2|4490:MT1B|4493:MT1E|4502:MT2A|4501:MT1X|4496:MT1H|4495:MT1G|4499:MT1M|4494:MT1F|475:ATOX1|10568:SLC34A2|113235:SLC46A1|490:ATP2B1|538:ATP7A|6546:SLC8A1	Localized autosomal recessive hypotrichosis|Idiopathic generalied epilepsies (IGEs)|Neurodegeneration with brain iron accumulation (NBIA)|Hartnup disorder|Distal hereditary motor neuropathies (dHMN)|Iminoglycinuria|Vitamin D-dependent rickets|Atransferrinemia|Congenital diarrhea|Hypochromic microcytic anemia|Hypomagnesemia		Minerals are one of the five fundamental groups of nutrients needed to sustain life. Of the minerals, calcium plays innumerable roles in our bodies, serving as a main component of bone as well as an intracellular messenger in muscle contraction/relaxation, neural networks, the immune system, and endocrine/exocrine cells. Iron, copper, and other metals are required for redox reactions (as cofactors) and for oxygen transport and binding (in hemoglobin and myoglobin). Many enzymes require specific metal atoms to complete their catalytic functions. Animal tissues need moderate quantities of some elements (Ca, P, K, Na, Mg, S, and Cl) and trace amounts of others (Mn, Fe, I, Co, Cr, Cu, Zn, and Se). The minerals are absorbed by either passive or active transport systems through the intestinal mucosa, often using specialized transport proteins, such as ferritin for Fe3+ and vitamin D-induced protein for calcium.
hsa00030	Pentose phosphate pathway - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	2821:GPI|2539:G6PD|25796:PGLS|9563:H6PD|5226:PGD|729020:rcRPE|6120:RPE|8277:TKTL1|7086:TKT|84076:TKTL2|6888:TALDO1|22934:RPIA|51071:DERA|64080:RBKS|5236:PGM1|55276:PGM2|5634:PRPS2|5631:PRPS1|221823:PRPS1L1|9104:RGN|229:ALDOB|230:ALDOC|226:ALDOA|8789:FBP2|2203:FBP1|5214:PFKP|5211:PFKL|5213:PFKM	Phosphoribosylpyrophosphate synthetase I superactivity|Anemia due to disorders of glutathione metabolism|Arts syndrome|Cortisone reductase deficiency (CRD)|Ribose 5-phosphate isomerase (RPI) deficiency|Transaldolase (TALDO) deficiency		The pentose phosphate pathway is a process of glucose turnover that produces NADPH as reducing equivalents and pentoses as essential parts of nucleotides. There are two different phases in the pathway. One is irreversible oxidative phase in which glucose-6P is converted to ribulose-5P by oxidative decarboxylation, and NADPH is generated [MD:M00006]. The other is reversible non-oxidative phase in which phosphorylated sugars are interconverted to generate xylulose-5P, ribulose-5P, and ribose-5P [MD:M00007]. Phosphoribosyl pyrophosphate (PRPP) formed from ribose-5P [MD:M00005] is an activated compound used in the biosynthesis of histidine and purine/pyrimidine nucleotides. This pathway map also shows the Entner-Doudoroff pathway where 6-P-gluconate is dehydrated and then cleaved into pyruvate and glyceraldehyde-3P [MD:M00008].
hsa00770	Pantothenate and CoA biosynthesis - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	53354:PANK1|55229:PANK4|79646:PANK3|80025:PANK2|79717:PPCS|60490:PPCDC|5169:ENPP3|5167:ENPP1|80347:COASY|60496:AASDHPPT|8875:VNN2|8876:VNN1|586:BCAT1|587:BCAT2|51733:UPB1|1807:DPYS|1806:DPYD	Core neuroacanthocytosis syndromes|Neurodegeneration with brain iron accumulation (NBIA)|Generalized arterial calcification of infancy	Gimeracil (JAN/INN)	
hsa00640	Propanoate metabolism - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	38:ACAT1|39:ACAT2|55902:ACSS2|84532:ACSS1|79611:ACSS3|34:ACADM|3030:HADHA|1962:EHHADH|1892:ECHS1|26275:HIBCH|31:ACACA|32:ACACB|23417:MLYCD|18:ABAT|5095:PCCA|5096:PCCB|84693:MCEE|4594:MUT|8802:SUCLG1|8801:SUCLG2|8803:SUCLA2|4329:ALDH6A1|219:ALDH1B1|224:ALDH3A2|217:ALDH2|501:ALDH7A1|223:ALDH9A1|92483:LDHAL6B|3948:LDHC|3939:LDHA|160287:LDHAL6A|3945:LDHB	Methylmalonic aciduria (MMA)|Propionic acidemia	Cyanamide (JP16)|Disulfiram (JP16/USP/INN)|Valproic acid (USP)|Vigabatrin (JAN/USAN/INN)|Sodium valproate (JP16)|Calcium valproate	
hsa05014	Amyotrophic lateral sclerosis (ALS) - Homo sapiens (human)	Human Diseases; Neurodegenerative Diseases	7157:TP53|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|834:CASP1|637:BID|596:BCL2|598:BCL2L1|581:BAX|572:BAD|317:APAF1|54205:CYCS|842:CASP9|836:CASP3|6647:SOD1|10452:TOMM40|84134:TOMM40L|79139:DERL1|4217:MAP3K5|7124:TNF|7132:TNFRSF1A|7133:TNFRSF1B|1616:DAXX|5606:MAP2K3|5608:MAP2K6|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|4842:NOS1|9973:CCS|847:CAT|5630:PRPH|5961:PRPH2|4747:NEFL|4741:NEFM|4744:NEFH|57679:ALS2|5868:RAB5A|5879:RAC1|6506:SLC1A2|2890:GRIA1|2891:GRIA2|2902:GRIN1|2903:GRIN2A|2904:GRIN2B|2905:GRIN2C|2906:GRIN2D|2876:GPX1	Amyotrophic lateral sclerosis (ALS)		Amyotrophic lateral sclerosis (ALS) is a progressive, lethal, degenerative disorder of motor neurons. The hallmark of this disease is the selective death of motor neurons in the brain and spinal cord, leading to paralysis of voluntary muscles. Mutant superoxide dismutase 1 (SOD1), as seen in some familial ALS (FALS) cases, is unstable, forming aggregates in the motor neuron cytoplasm, axoplasm and mitochondria. Within mitochondria, mutant SOD1 may interfere with the anti-apoptotic function of Bcl-2, affect mitochondrial import by interfering with the translocation machinery (TOM/TIM), and generate toxic free radicals (ROS). Reactive oxygen species (ROS), produced within mitochondria, inhibit the function of EAAT2, the main glial glutamate transporter protein, responsible for most of the reuptake of synaptically released glutamate. Glutamate excess increases intracellular calcium, which enhances oxidative stress and mitochondrial damage. Mutant SOD1 can also trigger oxidative reactions , which can then cause damage through the formation of hydroxyl radicals or via nitration of tyrosine residues on proteins. Nitration may target neurofilament proteins, affecting axonal transport. Collectively, these mechanisms are predicted to disturb cellular homeostasis, ultimately triggering motor neuron death.
hsa04110	Cell cycle - Homo sapiens (human)	Cellular Processes; Cell Growth and Death	595:CCND1|894:CCND2|896:CCND3|1019:CDK4|1021:CDK6|5925:RB1|5934:RBL2|5933:RBL1|25:ABL1|3066:HDAC2|3065:HDAC1|1871:E2F3|1869:E2F1|1870:E2F2|1874:E2F4|1875:E2F5|7027:TFDP1|7029:TFDP2|2932:GSK3B|7040:TGFB1|7042:TGFB2|7043:TGFB3|4087:SMAD2|4088:SMAD3|4089:SMAD4|4609:MYC|7709:ZBTB17|1029:CDKN2A|1030:CDKN2B|1031:CDKN2C|1032:CDKN2D|1027:CDKN1B|1028:CDKN1C|1026:CDKN1A|9134:CCNE2|898:CCNE1|1017:CDK2|6500:SKP1|8454:CUL1|9978:RBX1|6502:SKP2|890:CCNA2|8900:CCNA1|990:CDC6|8318:CDC45|8317:CDC7|10926:DBF4|983:CDK1|9133:CCNB2|891:CCNB1|85417:CCNB3|994:CDC25B|995:CDC25C|7529:YWHAB|7532:YWHAG|7533:YWHAH|10971:YWHAQ|7534:YWHAZ|7531:YWHAE|5347:PLK1|7465:WEE1|494551:WEE2|9088:PKMYT1|902:CCNH|1022:CDK7|64682:ANAPC1|29882:ANAPC2|996:CDC27|29945:ANAPC4|51433:ANAPC5|8881:CDC16|51434:ANAPC7|8697:CDC23|10393:ANAPC10|51529:ANAPC11|246184:CDC26|25847:ANAPC13|991:CDC20|10744:PTTG2|9232:PTTG1|9700:ESPL1|8243:SMC1A|27127:SMC1B|9126:SMC3|10274:STAG1|10735:STAG2|5885:RAD21|7272:TTK|699:BUB1|9184:BUB3|701:BUB1B|8379:MAD1L1|4085:MAD2L1|10459:MAD2L2|51343:FZR1|8556:CDC14A|8555:CDC14B|545:ATR|472:ATM|7157:TP53|1111:CHEK1|11200:CHEK2|1387:CREBBP|2033:EP300|5591:PRKDC|4193:MDM2|4616:GADD45B|1647:GADD45A|10912:GADD45G|5111:PCNA|2810:SFN|993:CDC25A|4998:ORC1|4999:ORC2|23595:ORC3|5000:ORC4|5001:ORC5|23594:ORC6|4171:MCM2|4172:MCM3|4173:MCM4|4174:MCM5|4175:MCM6|4176:MCM7	Type II diabetes mellitus|Cornelia de Lange syndrome (CdLS)|Beckwith-Wiedemann syndrome|Ataxia with ocular apraxia (AOA)|Li-Fraumeni syndrome|Seckel syndrome|Choroid plexus papilloma|Juvenile polyposis syndrome|Pituitary adenomas	Nilotinib hydrochloride hydrate (JAN)|Nilotinib (USAN/INN)	Mitotic cell cycle progression is accomplished through a reproducible sequence of events, DNA replication (S phase) and mitosis (M phase) separated temporally by gaps known as G1 and G2 phases. Cyclin-dependent kinases (CDKs) are key regulatory enzymes, each consisting of a catalytic CDK subunit and an activating cyclin subunit. CDKs regulate the cell's progression through the phases of the cell cycle by modulating the activity of key substrates. Downstream targets of CDKs include transcription factor E2F and its regulator Rb. Precise activation and inactivation of CDKs at specific points in the cell cycle are required for orderly cell division. Cyclin-CDK inhibitors (CKIs), such as p16Ink4a, p15Ink4b, p27Kip1, and p21Cip1, are involved in the negative regulation of CDK activities, thus providing a pathway through which the cell cycle is negatively regulated.|Eukaryotic cells respond to DNA damage by activating signaling pathways that promote cell cycle arrest and DNA repair. In response to DNA damage, the checkpoint kinase ATM phosphorylates and activates Chk2, which in turn directly phosphorylates and activates p53 tumor suppressor protein. p53 and its transcriptional targets play an important role in both G1 and G2 checkpoints. ATR-Chk1-mediated protein degradation of Cdc25A protein phosphatase is also a mechanism conferring intra-S-phase checkpoint activation.
hsa03010	Ribosome - Homo sapiens (human)	Genetic Information Processing; Translation	6187:RPS2|6188:RPS3|6189:RPS3A|6192:RPS4Y1|6191:RPS4X|6193:RPS5|6194:RPS6|6201:RPS7|6202:RPS8|6203:RPS9|6204:RPS10|6205:RPS11|6206:RPS12|6207:RPS13|6208:RPS14|6209:RPS15|6210:RPS15A|6217:RPS16|100505503:RPS17L|6218:RPS17|6222:RPS18|6223:RPS19|6224:RPS20|6227:RPS21|6228:RPS23|6229:RPS24|6230:RPS25|6231:RPS26|6232:RPS27|51065:RPS27L|6233:RPS27A|6234:RPS28|6235:RPS29|2197:FAU|3921:RPSA|28998:MRPL13|6123:RPL3L|6122:RPL3|6124:RPL4|6125:RPL5|6128:RPL6|6129:RPL7|6130:RPL7A|6132:RPL8|6133:RPL9|6134:RPL10|140801:RPL10L|4736:RPL10A|6135:RPL11|6136:RPL12|6137:RPL13|23521:RPL13A|9045:RPL14|6138:RPL15|6139:RPL17|6141:RPL18|6142:RPL18A|6143:RPL19|6144:RPL21|6146:RPL22|200916:RPL22L1|9349:RPL23|6147:RPL23A|6152:RPL24|51187:RSL24D1|6154:RPL26|51121:RPL26L1|6155:RPL27|6157:RPL27A|6158:RPL28|6159:RPL29|6156:RPL30|6160:RPL31|6161:RPL32|6164:RPL34|11224:RPL35|6165:RPL35A|25873:RPL36|6167:RPL37|6168:RPL37A|6169:RPL38|6170:RPL39|7311:UBA52|6171:RPL41|6173:RPL36A|6166:RPL36AL|6175:RPLP0|6176:RPLP1|6181:RPLP2|4549:RNR1|4550:RNR2	Diamond-Blackfan anemia (DBA)		
hsa05320	Autoimmune thyroid disease - Homo sapiens (human)	Human Diseases; Immune Diseases	3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|1493:CTLA4|7173:TPO|7038:TG|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|941:CD80|942:CD86|940:CD28|3558:IL2|3133:HLA-E|3134:HLA-F|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|356:FASLG|355:FAS|5551:PRF1|3002:GZMB|959:CD40LG|958:CD40|3565:IL4|3567:IL5|3586:IL10|100132941:uncharacterized|100291917:uncharacterized|7253:TSHR|1081:CGA|7252:TSHB	Hashimoto's thyroiditis|Graves' disease	Thiamazole (JP16/INN)|Propylthiouracil (JP16/USP/INN)|Methylthiouracil (INN)|Benzylthiouracil	The classification of autoimmune throid disease (AITD) includes Hashimoto's thyroiditis (HT) or chronic autoimmune thyroiditis and its variants,  Graves' disease (GD) and autoimmune atrophic thyroiditis or primary myxedema. HT is characterized by the presence of goitre, thyroid autoantibodies against thyroid peroxidase (TPO) and thyroglobulin (Tg) in serum and varying degrees of thyroid dysfunction. During HT, self-reactive CD4+ T lymphocytes (Th) recruit B cells and CD8+ T cells (CTL) into the thyroid. Disease progression leads to the death of thyroid cells and hypothyroidism. Both autoantibodies and thyroid-specific cytotoxic T lymphocytes (CTLs) have been proposed to be responsible for autoimmune thyrocyte depletion. In GD, the TSH-R is the most important autoantigen. Antibodies directed against it mimic the effects of the hormone on thyroid cells, TSH, stimulating autonomous production of thyroxine and triiodothyronine and causing hyperthyroidism. The presence of  TSH-R-blocking antibodies that bind the TSH receptor in a similar fashion to the antibodies in patients with Grave's disease but that block rather than activate the receptor explains some cases of atrophic hypothyroidism.
hsa00604	Glycosphingolipid biosynthesis - ganglio series - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	2583:B4GALNT1|8705:B3GALT4|6483:ST3GAL2|6482:ST3GAL1|29906:ST8SIA5|8869:ST3GAL5|6489:ST8SIA1|9197:SLC33A1|256435:ST6GALNAC3|27090:ST6GALNAC4|81849:ST6GALNAC5|30815:ST6GALNAC6|2720:GLB1|3073:HEXA|3074:HEXB	GM2 gangliosidoses|GM1 gangliosidosis|Amish infantile epilepsy syndrome		
hsa04623	Cytosolic DNA-sensing pathway - Homo sapiens (human)	Organismal Systems; Immune System	11128:POLR3A|55703:POLR3B|10623:POLR3C|661:POLR3D|55718:POLR3E|9533:POLR1C|51728:POLR3K|51082:POLR1D|171568:POLR3H|10622:POLR3G|84265:POLR3GL|10621:POLR3F|5434:POLR2E|5435:POLR2F|5437:POLR2H|5440:POLR2K|5441:POLR2L|23586:DDX58|57506:MAVS|4790:NFKB1|5970:RELA|3569:IL6|340061:TMEM173|29110:TBK1|9641:IKBKE|3661:IRF3|3665:IRF7|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3456:IFNB1|81030:ZBP1|8737:RIPK1|11035:RIPK3|8517:IKBKG|1147:CHUK|3551:IKBKB|4793:NFKBIB|4792:NFKBIA|9560:CCL4L1|388372:CCL4L2|6351:CCL4|6352:CCL5|3627:CXCL10|9447:AIM2|29108:PYCARD|834:CASP1|3553:IL1B|3606:IL18|90865:IL33|11277:TREX1|103:ADAR	Aicardi-Goutieres Syndrome (AGS)|Familial chilblain lupus (FCL)|Dyschromatosis symmetrica hereditaria|Cocoon syndrome|Retinal vasculopathy with cerebral leukodystrophy (RVCL)		Specific families of pattern recognition receptors are responsible for detecting foreign DNA from invading microbes or host cells and generating innate immune responses. DAI is the first identified sensor of cytosolic DNA which activates the IRF and NF-{kappa}B transcription factors, leading to production of type I interferon and other cytokines. The second type of cytoplasmic DNA sensor is AIM2. Upon sensing DNA, AIM2 triggers the assembly of the inflammasome, culminating in interleukin maturation. In addition to these receptors, there is a mechanism to sense foreign DNA, with the host RNA polymerase III converting the DNA into RNA for recognition by the RNA sensor RIG-I. These pathways provide various means to alert the cell.
hsa04666	Fc gamma R-mediated phagocytosis - Homo sapiens (human)	Organismal Systems; Immune System	100132941:uncharacterized|100291917:uncharacterized|2209:FCGR1A|9103:FCGR2C|2212:FCGR2A|5788:PTPRC|3055:HCK|4067:LYN|6850:SYK|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|6199:RPS6KB2|6198:RPS6KB1|5335:PLCG1|5336:PLCG2|5894:RAF1|5604:MAP2K1|5594:MAPK1|5595:MAPK3|4082:MARCKS|65108:MARCKSL1|5337:PLD1|5338:PLD2|8611:PPAP2A|8613:PPAP2B|8612:PPAP2C|8877:SPHK1|56848:SPHK2|5579:PRKCB|5578:PRKCA|5582:PRKCG|653361:NCF1|2934:GSN|85477:SCIN|10451:VAV3|7409:VAV1|7410:VAV2|998:CDC42|7454:WAS|8976:WASL|7408:VASP|10092:ARPC5|81873:ARPC5L|10093:ARPC4|10094:ARPC3|10095:ARPC1B|10552:ARPC1A|10109:ARPC2|5879:RAC1|5880:RAC2|8936:WASF1|10163:WASF2|10810:WASF3|5058:PAK1|3984:LIMK1|3985:LIMK2|1072:CFL1|1073:CFL2|8394:PIP5K1A|8395:PIP5K1B|23396:PIP5K1C|382:ARF6|1399:CRKL|1398:CRK|1794:DOCK2|50807:ASAP1|8853:ASAP2|55616:ASAP3|2213:FCGR2B|3635:INPP5D|9846:GAB2|27040:LAT|26052:DNM3|1785:DNM2|10059:DNM1L|1759:DNM1|273:AMPH|4651:MYO10|100137049:PLA2G4B|123745:PLA2G4E|2214:FCGR3A|255189:PLA2G4F|283748:PLA2G4D|5321:PLA2G4A|5580:PRKCD|5581:PRKCE|8398:PLA2G6|3636:INPPL1	Chronic granulomatous disease|Nemaline myopathy|Neurodegeneration with brain iron accumulation (NBIA)		Phagocytosis plays an essential role in host-defense mechanisms through the uptake and destruction of infectious pathogens. Specialized cell types including macrophages, neutrophils, and monocytes take part in this process in higher organisms. After opsonization with antibodies (IgG), foreign extracellular materials are recognized by Fc gamma receptors. Cross-linking of Fc gamma receptors initiates a variety of signals mediated by tyrosine phosphorylation of multiple proteins, which lead through the actin cytoskeleton rearrangements and membrane remodeling to the formation of phagosomes. Nascent phagosomes undergo a process of maturation that involves fusion with lysosomes. The acquisition of lysosomal proteases and release of reactive oxygen species are crucial for digestion of engulfed materials in phagosomes.
hsa00510	N-Glycan biosynthesis - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	22845:DOLK|1798:DPAGT1|29880:ALG5|79868:ALG13|199857:ALG14|8813:DPM1|8818:DPM2|54344:DPM3|56052:ALG1|85365:ALG2|440138:ALG11|91869:RFT1|10195:ALG3|79796:ALG9|79087:ALG12|29929:ALG6|79053:ALG8|144245:ALG10B|84920:ALG10|3703:STT3A|201595:STT3B|6184:RPN1|6185:RPN2|1603:DAD1|7991:TUSC3|1650:DDOST|57171:DOLPP1|7841:MOGS|23193:GANAB|57134:MAN1C1|4121:MAN1A1|10905:MAN1A2|11253:MAN1B1|4245:MGAT1|4122:MAN2A2|4124:MAN2A1|4247:MGAT2|2530:FUT8|2683:B4GALT1|8704:B4GALT2|8703:B4GALT3|6480:ST6GAL1|84620:ST6GAL2|4248:MGAT3|11282:MGAT4B|11320:MGAT4A|4249:MGAT5|146664:MGAT5B|25834:MGAT4C	Congenital disorders of glycosylation (CDG) type I|Congenital disorders of glycosylation (CDG) type II|Nonsyndromic autosomal recessive mental retardation (NS-ARMR)		N-glycans or asparagine-linked glycans are major constituents of glycoproteins in eukaryotes. N-glycans are covalently attached to asparagine with the consensus sequence of Asn-X-Ser/Thr by an N-glycosidic bond, GlcNAc b1- Asn. Biosynthesis of N-glycans begins on the cytoplasmic face of the ER membrane with the transferase reaction of UDP-GlcNAc and the lipid-like precursor P-Dol (dolichol phosphate) to generate GlcNAc a1- PP-Dol. After sequential addition of monosaccharides by ALG glycosyltransferases [MD:M00055], the N-glycan precursor is attached by the OST (oligosaccharyltransferase) complex to the polypeptide chain that is being synthesized and translocated through the ER membrane. The protein-bound N-glycan precursor is subsequently trimmed, extended, and modified in the ER and Golgi by a complex series of reactions catalyzed by membrane-bound glycosidases and glycosyltransferases. N-glycans thus synthesized are classified into three types: high-mannose type, complex type, and hybrid type. Defects in N-glycan biosynthesis lead to a variety of human diseases known as congenital disorders of glycosylation [DS:H00118 H00119].
hsa00563	Glycosylphosphatidylinositol(GPI)-anchor biosynthesis - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	5277:PIGA|5283:PIGH|5279:PIGC|9091:PIGQ|51227:PIGP|84992:PIGY|8818:DPM2|9487:PIGL|284098:PIGW|2822:GPLD1|93183:PIGM|54965:PIGX|55650:PIGV|23556:PIGN|9488:PIGB|5281:PIGF|84720:PIGO|8733:GPAA1|10026:PIGK|94005:PIGS|51604:PIGT|128869:PIGU|80055:PGAP1|80235:PIGZ|54872:PIGG	Paroxysmal nocturnal hemoglobinuria (PNH)|Glycosylphosphatidylinositol (GPI) deficiency		Cell surface proteins can be attached to the cell membrane via the glycolipid structure called glycosylphosphatidylinositol (GPI) anchor. Hundreds of GPI-anchored proteins have been identified in many eukaryotes ranging from protozoa and fungi to mammals. All protein-linked GPI anchors share a common core structure, characterized by the substructure Man (a1-4) GlcN (a1-6) myo-inositol-1P-lipid. Biosynthesis of GPI anchors proceeds in three stages: (i) preassembly of a GPI precursor in the ER membrane, (ii) attachment of the GPI to the C-terminus of a newly synthesized protein in the lumen of the ER, and (iii) lipid remodeling and/or carbohydrate side-chain modifications in the ER and the Golgi. Defects of GPI anchor biosynthesis gene result in a genetic disorder, paroxysmal nocturnal hemoglobinuria.
hsa00600	Sphingolipid metabolism - Homo sapiens (human)	Metabolism; Lipid Metabolism	9517:SPTLC2|10558:SPTLC1|55304:SPTLC3|2531:KDSR|29956:CERS2|10715:CERS1|204219:CERS3|91012:CERS5|79603:CERS4|253782:CERS6|427:ASAH1|56624:ASAH2|125981:ACER1|340485:ACER2|55331:ACER3|8560:DEGS1|123099:DEGS2|166929:SGMS2|259230:SGMS1|6609:SMPD1|6610:SMPD2|55512:SMPD3|55627:SMPD4|339221:ENPP7|64781:CERK|8611:PPAP2A|8613:PPAP2B|8612:PPAP2C|81537:SGPP1|130367:SGPP2|8877:SPHK1|56848:SPHK2|8879:SGPL1|7357:UGCG|2629:GBA|9331:B4GALT6|2720:GLB1|7368:UGT8|2581:GALC|9514:GAL3ST1|410:ARSA|4758:NEU1|10825:NEU3|4759:NEU2|129807:NEU4|2717:GLA	Fabry disease|Gaucher disease|Metachromatic leukodystrophy (MLD)|Krabbe disease|Niemann-Pick disease (NPD), including;|Farber lipogranulomatosis|Sialidosis|Galactosialidosis|GM1 gangliosidosis|Progressive myoclonic epilepsy (PME)	Miglustat (JAN/USAN/INN)	
hsa00260	Glycine, serine and threonine metabolism - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	6470:SHMT1|6472:SHMT2|5723:PSPH|29968:PSAT1|26227:PHGDH|132158:GLYCTK|5224:PGAM2|5223:PGAM1|441531:PGAM4|669:BPGM|23464:GCAT|211:ALAS1|212:ALAS2|4129:MAOB|4128:MAOA|314:AOC2|8639:AOC3|2731:GLDC|275:AMT|1738:DLD|1610:DAO|189:AGXT|64902:AGXT2|2628:GATM|2593:GAMT|55349:CHDH|501:ALDH7A1|635:BHMT|29958:DMGDH|51268:PIPOX|1757:SARDH|27232:GNMT|875:CBS|1491:CTH|10993:SDS|63826:SRR|9380:GRHPR	Primary hyperoxaluria (HP)|Cystathioninuria|Homocystinuria|Hypermethioninemia|Nonketotic hyperglycinemia|Guanidinoacetate methyltransferase (GAMT) deficiency|Creatine deficiency syndrome|Dimethylglycine dehydrogenase deficiency (DMGDHD)|3-Phosphoglycerate dehydrogenase (3-PGDH) deficiency|Phosphoserine aminotransferase (PSAT) deficiency	Isoniazid (JP16/USP/INN)|Phenelzine sulfate (USP)|Selegiline hydrochloride (JAN/USP)|Tranylcypromine sulfate (USP XXI)|Lazabemide hydrochloride (JAN/USAN)|Amezinium metilsulfate (JAN)|Isoniazid calcium pyruvinate (JAN)|Safrazine hydrochloride (JAN)|Isoniazid sodium methanesulfonate hydrate (JAN)|Toloxatone (INN)|Brofaromine (INN)|Moclobemide (USAN/INN)|Rasagiline mesylate (USAN)|Befloxatone (INN)|Pargyline hydrochloride (USAN)|Iproniazid (INN)|Isocarboxazid (INN)|Cimoxatone (INN)|Ladostigil tartrate (USAN)|Clorgiline (INN)|Caroxazone (USAN/INN)|Selegiline (USAN/INN)|Mofegiline hydrochloride (USAN)|Lazabemide (USAN/INN)|Milacemide hydrochloride (USAN)|Nialamide (INN)|Iproclozide (INN)|Iproniazid phosphate|Phenelzine (BAN)|Pargyline (INN)|Rasagiline (USAN/INN)|Tranylcypromine (INN)	Serine is derived from 3-phospho-D-glycerate, an intermediate of glycolysis [MD:M00020], and glycine is derived from serine. Threonine is an essential amino acid, which animals cannot synthesize. In bacteria and plants, threonine is derived from aspartate [MD:M00018].
hsa05211	Renal cell carcinoma - Homo sapiens (human)	Human Diseases; Cancers	3091:HIF1A|2034:EPAS1|112399:EGLN3|112398:EGLN2|54583:EGLN1|7428:VHL|6921:TCEB1|6923:TCEB2|9978:RBX1|8453:CUL2|405:ARNT|9915:ARNT2|1387:CREBBP|2033:EP300|6513:SLC2A1|7423:VEGFB|5228:PGF|7422:VEGFA|7424:VEGFC|2277:FIGF|7040:TGFB1|7042:TGFB2|7043:TGFB3|7039:TGFA|3082:HGF|4233:MET|2549:GAB1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|1399:CRKL|1398:CRK|2889:RAPGEF1|5906:RAP1A|5908:RAP1B|5781:PTPN11|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|3725:JUN|5879:RAC1|998:CDC42|5058:PAK1|5062:PAK2|5063:PAK3|10298:PAK4|56924:PAK6|57144:PAK7|2271:FH|201163:FLCN|2113:ETS1|5155:PDGFB	Renal cell carcinoma|von Hippel-Lindau syndrome	Sorafenib tosilate (JAN)|Sorafenib (USAN/INN)	Renal cell cancer (RCC) accounts for ~3% of human malignancies and its incidence appears to be rising. Although most cases of RCC seem to occur sporadically, an inherited predisposition to renal cancer accounts for 1-4% of cases. RCC is not a single disease, it has several morphological subtypes. Conventional RCC (clear cell RCC) accounts for ~80% of cases, followed by papillary RCC (10-15%), chromophobe RCC (5%), and collecting duct RCC (<1%). Genes potentially involved in sporadic neoplasms of each particular type are VHL, MET, BHD, and FH respectively. In the absence of VHL, hypoxia-inducible factor alpha (HIF-alpha) accumulates, leading to production of several growth factors, including vascular endothelial growth factor and platelet-derived growth factor. Activated MET mediates a number of biological effects including motility, invasion of extracellular matrix, cellular transformation, prevention of apoptosis and metastasis formation. Loss of functional FH leads to accumulation of fumarate in the cell, triggering inhibition of HPH and preventing targeted pVHL-mediated degradation of HIF-alpha. BHD mutations cause the Birt-Hogg-Dube syndrome and its associated chromophobe, hybrid oncocytic, and conventional (clear cell) RCC.
hsa00630	Glyoxylate and dicarboxylate metabolism - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	4190:MDH1|4191:MDH2|1431:CS|50:ACO2|48:ACO1|38:ACAT1|39:ACAT2|5095:PCCA|5096:PCCB|84693:MCEE|4594:MUT|51179:HAO2|54363:HAO1|9380:GRHPR|283871:PGP|81888:HYI|132158:GLYCTK|125061:AFMID|189:AGXT|2653:GCSH|2752:GLUL|6470:SHMT1|6472:SHMT2|847:CAT	Primary hyperoxaluria (HP)|Methylmalonic aciduria (MMA)		
hsa04210	Apoptosis - Homo sapiens (human)	Cellular Processes; Cell Growth and Death	356:FASLG|355:FAS|8743:TNFSF10|8793:TNFRSF10D|8794:TNFRSF10C|8795:TNFRSF10B|8797:TNFRSF10A|7124:TNF|7132:TNFRSF1A|3552:IL1A|3553:IL1B|3554:IL1R1|3556:IL1RAP|8772:FADD|8717:TRADD|8837:CFLAR|843:CASP10|841:CASP8|836:CASP3|840:CASP7|839:CASP6|330:BIRC3|331:XIAP|329:BIRC2|637:BID|596:BCL2|598:BCL2L1|54205:CYCS|317:APAF1|842:CASP9|1676:DFFA|1677:DFFB|9131:AIFM1|2021:ENDOG|472:ATM|7157:TP53|8737:RIPK1|7186:TRAF2|4615:MYD88|3654:IRAK1|3656:IRAK2|11213:IRAK3|51135:IRAK4|9020:MAP3K14|1147:CHUK|3551:IKBKB|8517:IKBKG|4792:NFKBIA|4790:NFKB1|5970:RELA|4803:NGF|4914:NTRK1|3562:IL3|3563:IL3RA|1439:CSF2RB|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|5573:PRKAR1A|5577:PRKAR2B|5576:PRKAR2A|5575:PRKAR1B|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|572:BAD|581:BAX|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|823:CAPN1|824:CAPN2|112401:BIRC8|79444:BIRC7	Autoimmune lymphoproliferative syndromes (ALPS)|PTEN hamartoma tumor syndrome (PHTS)|Osteoporosis, lymphedema, anhydrotic ectodermal dysplasia with immunodeficiency (OLEDAID)|Incontinentia pigmenti|Pyogenic bacterial infections, recurrent, due to MYD88 deficiency|Ataxia with ocular apraxia (AOA)|Li-Fraumeni syndrome|Cocoon syndrome|Tumor necrosis factor receptor-associated periodic syndrome (TRAPS)|Choroid plexus papilloma|Pituitary adenomas	Etanercept (genetical recombination) (JAN)|Adalimumab (genetical recombination) (JAN)|Infliximab (genetical recombination) (JAN)|Anakinra (USAN/INN)|Certolizumab pegol (genetical recombination) (JAN)|Daniplestim (USAN/INN)|Leridistim (USAN/INN)|Rilonacept (USAN/INN)	Apoptosis is a genetically controlled mechanisms of cell death involved in the regulation of tissue homeostasis. The 2 major pathways of apoptosis are the extrinsic (Fas and other TNFR superfamily members and ligands) and the intrinsic (mitochondria-associated) pathways, both of which are found in the cytoplasm. The extrinsic pathway is triggered by death receptor engagement, which initiates a signaling cascade mediated by caspase-8 activation. Caspase-8 both feeds directly into caspase-3 activation and stimulates the release of cytochrome c by the mitochondria. Caspase-3 activation leads to the degradation of cellular proteins necessary to maintain cell survival and integrity. The intrinsic pathway occurs when various apoptotic stimuli trigger the release of cytochrome c from the mitochondria (independently of caspase-8 activation). Cytochrome c interacts with Apaf-1 and caspase-9 to promote the activation of caspase-3. Recent studies point to the ER as a third subcellular compartment implicated in apoptotic execution. Alterations in Ca2+ homeostasis and accumulation of misfolded proteins in the ER cause ER stress. Prolonged ER stress can result in the activation of BAD and/or caspase-12, and execute apoptosis.
hsa03013	RNA transport - Homo sapiens (human)	Genetic Information Processing; Translation	10940:POP1|10557:RPP38|10775:POP4|51367:POP5|54913:RPP25|138716:RPP25L|10248:POP7|11102:RPP14|10556:RPP30|79897:RPP21|10799:RPP40|55520:ELAC1|60528:ELAC2|51095:TRNT1|5901:RAN|11260:XPOT|57510:XPO5|1917:EEF1A2|1915:EEF1A1|7514:XPO1|51808:PHAX|4686:NCBP1|22916:NCBP2|1207:CLNS1A|10419:PRMT5|96764:TGS1|3837:KPNB1|10073:SNUPN|51068:NMD3|84305:WIBG|7175:TPR|10762:NUP50|9972:NUP153|59343:SENP2|4928:NUP98|8480:RAE1|6396:SEC13|81929:SEH1L|55746:NUP133|57122:NUP107|79023:NUP37|23279:NUP160|79902:NUP85|348995:NUP43|23636:NUP62|9818:NUPL1|53371:NUP54|9688:NUP93|23165:NUP205|23511:NUP188|9631:NUP155|129401:NUP35|91181:NUP210L|23225:NUP210|55706:TMEM48|94026:POM121L2|9883:POM121|100101267:POM121C|8021:NUP214|4927:NUP88|5903:RANBP2|5905:RANGAP1|7329:UBE2I|6612:SUMO3|6613:SUMO2|387082:SUMO4|7341:SUMO1|8086:AAAS|11097:NUPL2|6607:SMN2|6606:SMN1|8487:GEMIN2|11218:DDX20|50628:GEMIN4|25929:GEMIN5|79833:GEMIN6|79760:GEMIN7|54960:GEMIN8|11171:STRAP|8669:EIF3J|8668:EIF3I|8667:EIF3H|8666:EIF3G|8665:EIF3F|3646:EIF3E|8664:EIF3D|8663:EIF3C|8662:EIF3B|8661:EIF3A|9086:EIF1AY|1964:EIF1AX|10289:EIF1B|10209:EIF1|1983:EIF5|1965:EIF2S1|8894:EIF2S2|1968:EIF2S3|1967:EIF2B1|8892:EIF2B2|8890:EIF2B4|8891:EIF2B3|8893:EIF2B5|9669:EIF5B|8672:EIF4G3|1982:EIF4G2|1981:EIF4G1|9470:EIF4E2|1977:EIF4E|253314:EIF4E1B|1974:EIF4A2|1973:EIF4A1|1975:EIF4B|340529:PABPC1L2A|645974:PABPC1L2B|5042:PABPC3|8761:PABPC4|26986:PABPC1|132430:PABPC4L|140886:PABPC5|80336:PABPC1L|10605:PAIP1|1978:EIF4EBP1|10460:TACC3|26999:CYFIP2|23191:CYFIP1|8087:FXR1|9513:FXR2|2332:FMR1|9939:RBM8A|4116:MAGOH|55110:MAGOHB|22794:CASC3|9775:EIF4A3|10284:SAP18|5411:PNN|22985:ACIN1|10921:RNPS1|10189:ALYREF|7919:DDX39B|9984:THOC1|57187:THOC2|8563:THOC5|79228:THOC6|80145:THOC7|84321:THOC3|10250:SRRM1|55998:NXF5|56000:NXF3|56001:NXF2|10482:NXF1|728343:NXF2B|55916:NXT2|29107:NXT1|5976:UPF1|26019:UPF2|65110:UPF3A|65109:UPF3B	Spinal muscular atrophy (SMA)|Fragile X Syndrome|Leukoencephalopathy with vanishing white matter|Infantile bilateral striatal necrosis (IBSN)		RNA transport from the nucleus to the cytoplasm is  fundamental for gene expression. The different RNA species that are produced in the nucleus are exported through the nuclear pore complexes (NPCs) via mobile export receptors. The majority of RNAs, such as tRNAs, rRNAs, and U snRNAs, are transported by specific export receptors, which belong to the karyopherin-beta family proteins. A feature of karyopherins is their regulation by the small GTPase Ran. However, general mRNA export is mechanistically different. Nuclear export of mRNAs is functionally coupled to different steps in gene expression processes, such as transcription, splicing, 3'-end formation and even translation.
hsa05131	Shigellosis - Homo sapiens (human)	Human Diseases; Infectious Diseases	3678:ITGA5|3688:ITGB1|960:CD44|391:RHOG|9844:ELMO1|1793:DOCK1|5879:RAC1|8936:WASF1|10163:WASF2|10092:ARPC5|81873:ARPC5L|10093:ARPC4|10094:ARPC3|10095:ARPC1B|10552:ARPC1A|10109:ARPC2|6714:SRC|3059:HCLS1|2017:CTTN|25:ABL1|1399:CRKL|1398:CRK|998:CDC42|7414:VCL|1729:DIAPH1|6093:ROCK1|9475:ROCK2|7454:WAS|8976:WASL|60:ACTB|71:ACTG1|375189:PFN4|5217:PFN2|5216:PFN1|345456:PFN3|9474:ATG5|10392:NOD1|64127:NOD2|8767:RIPK2|5602:MAPK10|5601:MAPK9|5599:MAPK8|5594:MAPK1|5595:MAPK3|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|8517:IKBKG|1147:CHUK|3551:IKBKB|4793:NFKBIB|4792:NFKBIA|4790:NFKB1|5970:RELA|3576:IL8|7307:U2AF1|23291:FBXW11|8945:BTRC|10459:MAD2L2|7322:UBE2D2	Shigellosis		Shigellosis, or bacillary dysentery, is an intestinal infection caused by Shigella, a genus of enterobacteria. Shigella are potential food-borne pathogens that are capable of colonizing the intestinal epithelium by exploiting epithelial-cell functions and circumventing the host innate immune response. During basolateral entry into the host-cell cytoplasm, Shigella deliver a subset of effectors into the host cells through the type III secretion system. The effectors induce membrane ruffling through the stimulation of the Rac1-WAVE-Arp2/3 pathway, enabling bacterial entry into the epithelial cells. During multiplication within the cells, Shigella secrete another subset of effectors. VirG induces actin polymerization at one pole of the bacteria, allowing the bacteria to spread intracellularly and to infect adjacent cells. OspF, OspG and IpaH(9.8) downregulate the production of proinflammatory cytokines such as IL-8, helping bacteria circumvent the innate immune response.
hsa04010	MAPK signaling pathway - Homo sapiens (human)	Environmental Information Processing; Signal Transduction	773:CACNA1A|774:CACNA1B|775:CACNA1C|776:CACNA1D|777:CACNA1E|778:CACNA1F|8913:CACNA1G|8912:CACNA1H|8911:CACNA1I|779:CACNA1S|781:CACNA2D1|9254:CACNA2D2|55799:CACNA2D3|93589:CACNA2D4|782:CACNB1|783:CACNB2|784:CACNB3|785:CACNB4|786:CACNG1|10369:CACNG2|10368:CACNG3|27092:CACNG4|27091:CACNG5|59285:CACNG6|59284:CACNG7|59283:CACNG8|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|5579:PRKCB|5578:PRKCA|5582:PRKCG|2768:GNA12|55970:GNG12|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|5923:RASGRF1|5924:RASGRF2|10125:RASGRP1|10235:RASGRP2|25780:RASGRP3|115727:RASGRP4|9693:RAPGEF2|4763:NF1|5921:RASA1|5922:RASA2|5906:RAP1A|5908:RAP1B|4803:NGF|627:BDNF|4908:NTF3|4909:NTF4|1950:EGF|2258:FGF13|2253:FGF8|8817:FGF18|2257:FGF12|2248:FGF3|2251:FGF6|2256:FGF11|8823:FGF16|2252:FGF7|2259:FGF14|8822:FGF17|9965:FGF19|2254:FGF9|2250:FGF5|2249:FGF4|8074:FGF23|27006:FGF22|26281:FGF20|2255:FGF10|2247:FGF2|26291:FGF21|2246:FGF1|5154:PDGFA|5155:PDGFB|4914:NTRK1|4915:NTRK2|1956:EGFR|2260:FGFR1|2263:FGFR2|2261:FGFR3|2264:FGFR4|5156:PDGFRA|5159:PDGFRB|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|6237:RRAS|22800:RRAS2|22808:MRAS|673:BRAF|5894:RAF1|4342:MOS|5604:MAP2K1|5605:MAP2K2|8649:LAMTOR3|5594:MAPK1|5595:MAPK3|8569:MKNK1|2872:MKNK2|6195:RPS6KA1|6196:RPS6KA2|6197:RPS6KA3|27330:RPS6KA6|468:ATF4|2002:ELK1|2005:ELK4|4609:MYC|6722:SRF|2353:FOS|4137:MAPT|3925:STMN1|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|7124:TNF|3552:IL1A|3553:IL1B|7040:TGFB1|7042:TGFB2|7043:TGFB3|7132:TNFRSF1A|3554:IL1R1|7850:IL1R2|7046:TGFBR1|7048:TGFBR2|356:FASLG|355:FAS|929:CD14|5879:RAC1|5880:RAC2|5881:RAC3|998:CDC42|836:CASP3|7186:TRAF2|1616:DAXX|7189:TRAF6|4616:GADD45B|1647:GADD45A|10912:GADD45G|10454:TAB1|23118:TAB2|51295:ECSIT|8491:MAP4K3|9448:MAP4K4|11184:MAP4K1|5058:PAK1|5062:PAK2|6789:STK4|6788:STK3|5871:MAP4K2|1326:MAP3K8|4214:MAP3K1|4296:MAP3K11|10746:MAP3K2|4215:MAP3K3|9175:MAP3K13|7786:MAP3K12|51776:ZAK|9064:MAP3K6|4217:MAP3K5|6885:MAP3K7|4216:MAP3K4|9344:TAOK2|57551:TAOK1|51347:TAOK3|6416:MAP2K4|5609:MAP2K7|5606:MAP2K3|5608:MAP2K6|9479:MAPK8IP1|23542:MAPK8IP2|23162:MAPK8IP3|2317:FLNB|2318:FLNC|2316:FLNA|1399:CRKL|1398:CRK|409:ARRB2|408:ARRB1|5602:MAPK10|5601:MAPK9|5599:MAPK8|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|8550:MAPKAPK5|9261:MAPKAPK2|7867:MAPKAPK3|9252:RPS6KA5|8986:RPS6KA4|994:CDC25B|3725:JUN|3727:JUND|1386:ATF2|7157:TP53|1649:DDIT3|4149:MAX|4208:MEF2C|3315:HSPB1|207:AKT1|208:AKT2|10000:AKT3|5494:PPM1A|5801:PTPRR|84867:PTPN5|5778:PTPN7|1849:DUSP7|1847:DUSP5|1852:DUSP9|1846:DUSP4|1848:DUSP6|1845:DUSP3|1844:DUSP2|1850:DUSP8|56940:DUSP22|11072:DUSP14|11221:DUSP10|80824:DUSP16|1843:DUSP1|5536:PPP5C|5495:PPM1B|3306:HSPA2|3310:HSPA6|3304:HSPA1B|3305:HSPA1L|3312:HSPA8|3303:HSPA1A|2122:MECOM|5607:MAP2K5|5598:MAPK7|3164:NR4A1|9020:MAP3K14|1147:CHUK|3551:IKBKB|8517:IKBKG|51701:NLK|4790:NFKB1|4791:NFKB2|5970:RELA|5971:RELB|4773:NFATC2|4776:NFATC4	Frontotemporal lobar degeneration (FTLD)|Noonan syndrome and related disorders|RASA1-related disorders|PTEN hamartoma tumor syndrome (PHTS)|Osteoporosis, lymphedema, anhydrotic ectodermal dysplasia with immunodeficiency (OLEDAID)|Coffin-Lowry syndrome (CLS)|Syndromic X-linked mental retardation with epilepsy or seizures|Myofibrillar myopathies (MFM)|Lacrimo-auriculo-dento-digital syndrome (LADD)|Incontinentia pigmenti|Aplasia of lacrimal and salivary glands|Brugada syndrome (BRS)|Hypokalemic periodic paralysis (HypoPP)|Episodic ataxias|Familial or sporadic hemiplegic migraine|Congenital stationary night blindness (CSNB)|Loeys-Dietz syndrome (LDS)|Familial thoracic aortic aneurysm and dissection (TAAD)|Idiopathic generalied epilepsies (IGEs)|Distal hereditary motor neuropathies (dHMN)|Li-Fraumeni syndrome|Cocoon syndrome|FG syndrome (FGS)|Tumor necrosis factor receptor-associated periodic syndrome (TRAPS)|Congenital central hypoventilation syndrome (CCHS)|CATSHL syndrome|Choroid plexus papilloma|Familial tumoral calcinosis (FTC)|Trigonocephaly	Divalproex sodium (USP)|Felodipine (JAN/USP/INN)|Gabapentin (JAN/USAN/INN)|Isradipine (USP/INN)|Valproic acid (USP)|Nifedipine (JP16/USP/INN)|Nimodipine (USAN/INN)|Zonisamide (JAN/USAN/INN)|Ethosuximide (JP16/USP/INN)|Amlodipine besilate (JP16)|Diltiazem hydrochloride (JP16/USP)|Nicardipine hydrochloride (JP16/USAN)|Nisoldipine (JAN/USAN/INN)|Verapamil hydrochloride (JP16/USP)|Nitrendipine (JP16/USAN/INN)|Bepridil hydrochloride hydrate (JAN)|Sodium valproate (JP16)|Etanercept (genetical recombination) (JAN)|Barnidipine hydrochloride (JAN)|Azelnidipine (JAN/INN)|Cilnidipine (JAN/INN)|Flunarizine hydrochloride (JAN/USAN)|Imatinib mesilate (JAN)|Manidipine hydrochloride (JP16)|Aranidipine (JAN/INN)|Efonidipine hydrochloride ethanolate (JAN)|Nilvadipine (JP16/USAN/INN)|Gallopamil hydrochloride (JAN)|Gefitinib (JAN/USAN/INN)|Benidipine hydrochloride (JP16)|Verapamil (USAN/INN)|Dronedarone (INN)|Adalimumab (genetical recombination) (JAN)|Infliximab (genetical recombination) (JAN)|Penfluridol (USAN/INN)|Pregabalin (JAN/USAN/INN)|Amlodipine maleate (USAN)|Anakinra (USAN/INN)|Becaplermin (USAN/INN)|Axitinib (JAN/USAN)|Canertinib dihydrochloride (USAN)|Certolizumab pegol (genetical recombination) (JAN)|Cetuximab (genetical recombination) (JAN)|Darodipine (USAN/INN)|Dasatinib (INN)|Diltiazem malate (USAN)|Dronedarone hydrochloride (USAN)|Erlotinib hydrochloride (JAN/USAN)|Lapatinib tosilate hydrate (JAN)|Golimumab (genetical recombination) (JAN)|Lacidipine (USAN/INN)|Lestaurtinib (USAN/INN)|Mibefradil dihydrochloride (USAN)|Midostaurin (USAN/INN)|Panitumumab (genetical recombination) (JAN)|Pazopanib hydrochloride (JAN/USAN)|Pelitinib (USAN/INN)|Tandutinib (USAN/INN)|Sorafenib tosilate (JAN)|Vatalanib (USAN/INN)|Sunitinib malate (JAN/USAN)|Vandetanib (JAN/USAN/INN)|Nilotinib hydrochloride hydrate (JAN)|Dasatinib hydrate (JAN)|Rilonacept (USAN/INN)|Motesanib|Amlodipine (INN)|Barnidipine (INN)|Benidipine (INN)|Bepridil (INN)|Diltiazem (INN)|Efonidipine (INN)|Erlotinib (INN)|Flunarizine (INN)|Gallopamil (INN)|Imatinib (INN)|Lapatinib (INN)|Manidipine (INN)|Mibefradil (INN)|Nicardipine (INN)|Sorafenib (USAN/INN)|Sunitinib (INN)|Calcium valproate|Cediranib (USAN/INN)|Cediranib maleate (JAN/USAN)|Motesanib diphosphate (USAN)|Neratinib (INN/USAN)|Nilotinib (USAN/INN)|Canakinumab (genetical recombination) (JAN)|Gabapentin enacarbil (JAN/USAN/INN)|Afatinib (USAN/INN)|Afatinib maleate (JAN)|Lenvatinib (USAN/INN)|Lenvatinib mesylate (USAN)|Zalutumumab (USAN/INN)|Cabozantinib (USAN)|Crenolanib (USAN)|Crenolanib besylate (USAN)|Regorafenib (USAN/INN)	The mitogen-activated protein kinase (MAPK) cascade is a highly conserved module that is involved in various cellular functions, including cell proliferation, differentiation and migration. Mammals express at least four distinctly regulated groups of MAPKs, extracellular signal-related kinases (ERK)-1/2, Jun amino-terminal kinases (JNK1/2/3), p38 proteins (p38alpha/beta/gamma/delta) and ERK5, that are activated by specific MAPKKs: MEK1/2 for ERK1/2, MKK3/6 for the p38, MKK4/7 (JNKK1/2) for the JNKs, and MEK5 for ERK5. Each MAPKK, however, can be activated by more than one MAPKKK, increasing the complexity and diversity of MAPK signalling. Presumably each MAPKKK confers responsiveness to distinct stimuli. For example, activation of ERK1/2 by growth factors depends on the MAPKKK c-Raf, but other MAPKKKs may activate ERK1/2 in response to pro-inflammatory stimuli.
hsa01040	Biosynthesis of unsaturated fatty acids - Homo sapiens (human)	Metabolism; Lipid Metabolism	79071:ELOVL6|51144:HSD17B12|55825:PECR|201562:PTPLB|9200:PTPLA|9524:TECR|6319:SCD|79966:SCD5|9415:FADS2|60481:ELOVL5|3992:FADS1|54898:ELOVL2|8310:ACOX3|51:ACOX1|3030:HADHA|30:ACAA1|122970:ACOT4|641371:ACOT1|10965:ACOT2|11332:ACOT7|570:BAAT	Peroxisomal beta-oxidation enzyme deficiency		
hsa00564	Glycerophospholipid metabolism - Homo sapiens (human)	Metabolism; Lipid Metabolism	2819:GPD1|23171:GPD1L|2820:GPD2|150763:GPAT2|57678:GPAM|137964:AGPAT6|84803:AGPAT9|10554:AGPAT1|10555:AGPAT2|253558:LCLAT1|129642:MBOAT2|154141:MBOAT1|56895:AGPAT4|56894:AGPAT3|8443:GNPAT|56985:C17orf48|8611:PPAP2A|8613:PPAP2B|8612:PPAP2C|8525:DGKZ|1607:DGKB|1609:DGKQ|1608:DGKG|9162:DGKI|8527:DGKD|1606:DGKA|8526:DGKE|160851:DGKH|56994:CHPT1|10390:CEPT1|5337:PLD1|5338:PLD2|3931:LCAT|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|151056:PLB1|54947:LPCAT2|79888:LPCAT1|254531:LPCAT4|10162:LPCAT3|10434:LYPLA1|23659:PLA2G15|11313:LYPLA2|10908:PNPLA6|375775:PNPLA7|1103:CHAT|43:ACHE|1119:CHKA|1120:CHKB|162466:PHOSPHO1|5130:PCYT1A|9468:PCYT1B|85465:EPT1|55224:ETNK2|55500:ETNK1|5833:PCYT2|10400:PEMT|1040:CDS1|8760:CDS2|9791:PTDSS1|81490:PTDSS2|23761:PISD|9489:PGS1|54675:CRLS1|6901:TAZ|9926:LPGAT1|10423:CDIPT|79143:MBOAT7|23175:LPIN1|64900:LPIN3|9663:LPIN2	Lecithin:cholesterol acyltransferase deficiency|Rhizomelic chondrodysplasia punctata|Barth syndrome (BTHS)|Congenital myasthenic syndrome|Neurodegeneration with brain iron accumulation (NBIA)|Majeed syndrome	Isoflurophate (USP)|Physostigmine (USP)|Pralidoxime chloride (USP)|Pyridostigmine bromide (JP16/USP/INN)|Malathion (USP)|Demecarium bromide (USP/INN)|Donepezil hydrochloride (JP16/USAN)|Edrophonium chloride (JP16/USP/INN)|Neostigmine bromide (JAN/USP/INN)|Neostigmine methylsulfate (JP16/USP)|Ambenonium chloride (JP16/INN)|Distigmine bromide (JP16/INN)|Pralidoxime iodide (JAN/USAN)|Tacrine hydrochloride (USP)|Galantamine hydrobromide (JAN/USAN)|Ecothiopate iodide (JP16/INN)|Physostigmine salicylate (JAN/USP)|Rivastigmine tartrate|Dimetacrine (INN)|Itopride hydrochloride (JAN)|Besipirdine hydrochloride (USAN)|Ladostigil tartrate (USAN)|Icopezil maleate (USAN)|Dichlorvos (USAN/INN)|Rivastigmine (JAN/USAN/INN)|Physostigmine sulfate (USP)|Galantamine (USAN/INN)|Obidoxime chloride (USAN)|Pralidoxime mesylate (USAN)|Velnacrine maleate (USAN)|Donepezil (INN)|Neostigmine (BAN)|Tacrine (INN)	
hsa05218	Melanoma - Homo sapiens (human)	Human Diseases; Cancers	2258:FGF13|2253:FGF8|8817:FGF18|2257:FGF12|2248:FGF3|2251:FGF6|2256:FGF11|8823:FGF16|2252:FGF7|2259:FGF14|8822:FGF17|9965:FGF19|2254:FGF9|2250:FGF5|2249:FGF4|8074:FGF23|27006:FGF22|26281:FGF20|2255:FGF10|2247:FGF2|26291:FGF21|2246:FGF1|3082:HGF|3479:IGF1|5154:PDGFA|5155:PDGFB|56034:PDGFC|80310:PDGFD|1950:EGF|2260:FGFR1|4233:MET|3480:IGF1R|5156:PDGFRA|5159:PDGFRB|1956:EGFR|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|1019:CDK4|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|572:BAD|5728:PTEN|1029:CDKN2A|4193:MDM2|7157:TP53|1026:CDKN1A|595:CCND1|1021:CDK6|5925:RB1|1871:E2F3|1869:E2F1|1870:E2F2|999:CDH1|4286:MITF	Malignant melanoma	Vemurafenib (USAN/INN)	Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations.  Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression.
hsa04330	Notch signaling pathway - Homo sapiens (human)	Environmental Information Processing; Signal Transduction	28514:DLL1|10683:DLL3|54567:DLL4|3714:JAG2|182:JAG1|5986:RFNG|3955:LFNG|4242:MFNG|4854:NOTCH3|4853:NOTCH2|4855:NOTCH4|4851:NOTCH1|11317:RBPJL|3516:RBPJ|3280:HES1|388585:HES5|171558:PTCRA|1856:DVL2|1857:DVL3|1855:DVL1|9253:NUMBL|8650:NUMB|1840:DTX1|23220:DTX4|113878:DTX2|151636:DTX3L|196403:DTX3|6868:ADAM17|5663:PSEN1|5664:PSEN2|55851:PSENEN|23385:NCSTN|51107:APH1A|55534:MAML3|84441:MAML2|9794:MAML1|1387:CREBBP|2033:EP300|8850:KAT2B|2648:KAT2A|22938:SNW1|1488:CTBP2|1487:CTBP1|9612:NCOR2|9541:CIR1|3066:HDAC2|3065:HDAC1	Frontotemporal lobar degeneration (FTLD)|Spondylocostal dysostosis (SCD)|Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL)|Tetralogy of Fallot|Alagille syndrome|Bicuspid aortic valve|Hajdu-Cheney syndrome|Acne inversa	Begacestat (USAN/INN)|Tarenflurbil (INN/USAN)|Semagacestat (USAN/INN)|Avagacestat (USAN)	The Notch signaling pathway is an evolutionarily conserved, intercellular signaling mechanism essential for proper embryonic development in all metazoan organisms in the Animal kingdom. The Notch proteins (Notch1-Notch4 in vertebrates) are single-pass receptors that are activated by the Delta (or Delta-like) and Jagged/Serrate families of membrane-bound ligands. They are transported to the plasma membrane as cleaved, but otherwise intact polypeptides. Interaction with ligand leads to two additional proteolytic cleavages that liberate the Notch intracellular domain (NICD) from the plasma membrane. The NICD translocates to the nucleus, where it forms a complex with the DNA binding protein CSL, displacing a histone deacetylase (HDAc)-co-repressor (CoR) complex from CSL. Components of an activation complex, such as MAML1 and histone acetyltransferases (HATs), are recruited to the NICD-CSL complex, leading to the transcriptional activation of Notch target genes.
hsa00400	Phenylalanine, tyrosine and tryptophan biosynthesis - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	2805:GOT1|2806:GOT2|6898:TAT|259307:IL4I1|5053:PAH	Phenylketonuria (PKU)		
hsa04612	Antigen processing and presentation - Homo sapiens (human)	Organismal Systems; Immune System	3458:IFNG|7124:TNF|5720:PSME1|5721:PSME2|10197:PSME3|3306:HSPA2|3310:HSPA6|3304:HSPA1B|3305:HSPA1L|3312:HSPA8|3303:HSPA1A|3308:HSPA4|3320:HSP90AA1|3326:HSP90AB1|3133:HLA-E|3134:HLA-F|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|821:CANX|567:B2M|2923:PDIA3|811:CALR|6892:TAPBP|6890:TAP1|6891:TAP2|925:CD8A|926:CD8B|115653:KIR3DL3|3812:KIR3DL2|3811:KIR3DL1|3805:KIR2DL4|3803:KIR2DL2|57292:KIR2DL5A|3802:KIR2DL1|3804:KIR2DL3|3822:KLRC2|3823:KLRC3|8302:KLRC4|3821:KLRC1|3824:KLRD1|3806:KIR2DS1|3810:KIR2DS5|3809:KIR2DS4|3808:KIR2DS3|10437:IFI30|5641:LGMN|1508:CTSB|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|972:CD74|1514:CTSL1|1520:CTSS|920:CD4|4261:CIITA|5993:RFX5|8625:RFXANK|5994:RFXAP|1385:CREB1|4800:NFYA|4801:NFYB|4802:NFYC|3309:HSPA5	Leprosy|Tropical calcific pancreatitis|Bare lymphocyte syndrome (BLS) type1|Bare lymphocyte syndrome (BLS) type2|Aplastic anemia (AA)	Etanercept (genetical recombination) (JAN)|Adalimumab (genetical recombination) (JAN)|Infliximab (genetical recombination) (JAN)|Certolizumab pegol (genetical recombination) (JAN)	
hsa04360	Axon guidance - Homo sapiens (human)	Organismal Systems; Development	9423:NTN1|1630:DCC|5879:RAC1|5880:RAC2|5881:RAC3|22885:ABLIM3|84448:ABLIM2|3983:ABLIM1|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|4776:NFATC4|4772:NFATC1|4773:NFATC2|4775:NFATC3|10725:NFAT5|387:RHOA|6093:ROCK1|9475:ROCK2|8633:UNC5C|219699:UNC5B|90249:UNC5A|137970:UNC5D|4917:NTN3|59277:NTN4|22854:NTNG1|57689:LRRC4C|1946:EFNA5|1943:EFNA2|1945:EFNA4|1944:EFNA3|1942:EFNA1|2534:FYN|1949:EFNB3|1948:EFNB2|1947:EFNB1|5747:PTK2|5998:RGS3|2041:EPHA1|1969:EPHA2|2042:EPHA3|2043:EPHA4|2044:EPHA5|285220:EPHA6|2045:EPHA7|2046:EPHA8|2047:EPHB1|2048:EPHB2|2049:EPHB3|2050:EPHB4|2051:EPHB6|25:ABL1|25791:NGEF|998:CDC42|5058:PAK1|5062:PAK2|5063:PAK3|10298:PAK4|56924:PAK6|57144:PAK7|5921:RASA1|3265:HRAS|3845:KRAS|4893:NRAS|5594:MAPK1|5595:MAPK3|7852:CXCR4|2773:GNAI3|2770:GNAI1|2771:GNAI2|6585:SLIT1|9353:SLIT2|6586:SLIT3|6091:ROBO1|6092:ROBO2|64221:ROBO3|9901:SRGAP3|57522:SRGAP1|23380:SRGAP2|10512:SEMA3C|7869:SEMA3B|6405:SEMA3F|9723:SEMA3E|56920:SEMA3G|10371:SEMA3A|223117:SEMA3D|5362:PLXNA2|5361:PLXNA1|55558:PLXNA3|8829:NRP1|3897:L1CAM|2932:GSK3B|1020:CDK5|2242:FES|1808:DPYSL2|56896:DPYSL5|3984:LIMK1|3985:LIMK2|1072:CFL1|1073:CFL2|29984:RHOD|27289:RND1|10505:SEMA4F|54910:SEMA4C|57715:SEMA4G|10507:SEMA4D|10509:SEMA4B|64218:SEMA4A|9037:SEMA5A|54437:SEMA5B|10500:SEMA6C|57556:SEMA6A|80031:SEMA6D|10501:SEMA6B|5365:PLXNB3|5364:PLXNB1|23654:PLXNB2|4233:MET|23365:ARHGEF12|8482:SEMA7A|3688:ITGB1|10154:PLXNC1|4690:NCK1|6387:CXCL12|8440:NCK2	Syndromic X-linked mental retardation with epilepsy or seizures|Nemaline myopathy|Cri du chat syndrome|L1 syndrome	Valategrast hydrochloride (USAN)	Axon guidance represents a key stage in the formation of neuronal network. Axons are guided by a variety of guidance factors, such as netrins, ephrins, Slits, and semaphorins. These guidance cues are read by growth cone receptors, and signal transduction pathways downstream of these receptors converge onto the Rho GTPases to elicit changes in cytoskeletal organization that determine which way the growth cone will turn.
hsa00760	Nicotinate and nicotinamide metabolism - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	23475:QPRT|93100:NAPRT1|4860:PNP|54981:C9orf95|27231:ITGB1BP3|4907:NT5E|22978:NT5C2|51251:NT5C3|56953:NT5M|30833:NT5C|93034:NT5C1B|84618:NT5C1A|23057:NMNAT2|64802:NMNAT1|349565:NMNAT3|5169:ENPP3|5167:ENPP1|83594:NUDT12|55191:NADSYN1|10135:NAMPT|683:BST1|952:CD38|65220:NADK|23530:NNT|4837:NNMT|316:AOX1	Calcification of joints and arteries|Generalized arterial calcification of infancy	Forodesine hydrochloride (JAN/USAN)|Forodesine (USAN/INN)	
hsa00270	Cysteine and methionine metabolism - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	1491:CTH|635:BHMT|4548:MTR|4144:MAT2A|4143:MAT1A|27430:MAT2B|262:AMD1|6723:SRM|6611:SMS|4507:MTAP|84245:MRI1|51074:APIP|58478:ENOPH1|55256:ADI1|6898:TAT|259307:IL4I1|1789:DNMT3B|29947:DNMT3L|1786:DNMT1|1788:DNMT3A|191:AHCY|23382:AHCYL2|10768:AHCYL1|875:CBS|1036:CDO1|2805:GOT1|2806:GOT2|4357:MPST|7263:TST|92483:LDHAL6B|3948:LDHC|3939:LDHA|160287:LDHAL6A|3945:LDHB|10993:SDS	Sialuria/ Sialic acid storage disease|Cystathioninuria|Homocystinuria|Hypermethioninemia|Snyder-Robinson syndrome		Cysteine and methionine are sulfur-containing amino acids. Cysteine is synthesized from serine through different pathways in different organism groups. In bacteria and plants, cysteine is converted from serine (via acetylserine) by transfer of hydrogen sulfide [MD:M00021]. In animals, methionine-derived homocysteine is used as sulfur source and its condensation product with serine (cystathionine) is converted to cysteine [MD:M00338]. Cysteine is metabolized to pyruvate in multiple routes. Methionine is an essential amino acid, which animals cannot synthesize. In bacteria and plants, methionine is synthesized from aspartate [MD:M00017]. S-Adenosylmethionine (SAM), synthesized from methionine and ATP, is a methyl group donor in many important transfer reactions including DNA methylation for regulation of gene expression. SAM may also be used to regenerate methionine in the methionine salvage pathway [MD:M00034].
hsa05216	Thyroid cancer - Homo sapiens (human)	Human Diseases; Cancers	5979:RET|8030:CCDC6|8031:NCOA4|4914:NTRK1|7170:TPM3|7175:TPR|10342:TFG|3265:HRAS|4893:NRAS|3845:KRAS|673:BRAF|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|7849:PAX8|5468:PPARG|6256:RXRA|6257:RXRB|6258:RXRG|7157:TP53|999:CDH1|1499:CTNNB1|6932:TCF7|83439:TCF7L1|6934:TCF7L2|51176:LEF1|4609:MYC|595:CCND1	Thyroid cancer		Thyroid cancer is the most common endocrine malignancy and accounts for the majority of endocrine cancer- related deaths each year. More than 95% of thyroid carcinomas are derived from follicular cells.  Their behavior varies from the indolent growing, well-differentiated papillary and follicular carcinomas (PTC and FTC, respectively) to the extremely aggressive undifferentiated carcinoma (UC). Somatic rearrangements of RET and TRK are almost exclusively found in PTC and may be found in early stages. The most distinctive molecular features of FTC are the prominence of aneuploidy and the high prevalence of RAS mutations and PAX8-PPAR{gamma} rearrangements. p53 seems to play a crucial role in the dedifferentiation process of thyroid carcinoma.
hsa03022	Basal transcription factors - Homo sapiens (human)	Genetic Information Processing; Transcription	2957:GTF2A1|11036:GTF2A1L|2958:GTF2A2|2959:GTF2B|387332:TBPL2|9519:TBPL1|6908:TBP|6872:TAF1|138474:TAF1L|6873:TAF2|54457:TAF7L|6879:TAF7|129685:TAF8|83860:TAF3|6881:TAF10|6877:TAF5|27097:TAF5L|6874:TAF4|6875:TAF4B|6883:TAF12|6878:TAF6|10629:TAF6L|6880:TAF9|51616:TAF9B|6882:TAF11|6884:TAF13|8148:TAF15|2960:GTF2E1|2961:GTF2E2|2962:GTF2F1|2963:GTF2F2|2965:GTF2H1|2966:GTF2H2|728340:GTF2H2C|730394:GTF2H2D|2967:GTF2H3|2968:GTF2H4|2071:ERCC3|2068:ERCC2|404672:GTF2H5|1022:CDK7|4331:MNAT1|902:CCNH|9569:GTF2IRD1|2969:GTF2I			
hsa04974	Protein digestion and absorption - Homo sapiens (human)	Organismal Systems; Digestive System	5222:PGA5|643834:PGA3|643847:PGA4|5646:PRSS3|5645:PRSS2|5644:PRSS1|1506:CTRL|51032:CELA2B|63036:CELA2A|10136:CELA3A|23436:CELA3B|1357:CPA1|1358:CPA2|1359:CPA3|1360:CPB1|1361:CPB2|6550:SLC9A3|6564:SLC15A1|476:ATP1A1|480:ATP1A4|478:ATP1A3|477:ATP1A2|481:ATP1B1|482:ATP1B2|483:ATP1B3|23439:ATP1B4|486:FXYD2|3783:KCNN4|8645:KCNK5|10008:KCNE3|3784:KCNQ1|3769:KCNJ13|54407:SLC38A2|4311:MME|4224:MEP1A|4225:MEP1B|59272:ACE2|5547:PRCP|1803:DPP4|7512:XPNPEP2|6505:SLC1A1|6510:SLC1A5|6547:SLC8A3|6546:SLC8A1|6543:SLC8A2|340024:SLC6A19|6520:SLC3A2|23428:SLC7A8|117247:SLC16A10|6519:SLC3A1|11136:SLC7A9|9056:SLC7A7|2006:ELN|1280:COL2A1|1302:COL11A2|1301:COL11A1|1277:COL1A1|1289:COL5A1|50509:COL5A3|1281:COL3A1|1290:COL5A2|1278:COL1A2|1284:COL4A2|1286:COL4A4|1288:COL4A6|1287:COL4A5|1282:COL4A1|1292:COL6A2|1291:COL6A1|1293:COL6A3|131873:COL6A6|1297:COL9A1|1298:COL9A2|1299:COL9A3|1303:COL12A1|7373:COL14A1|1306:COL15A1|1308:COL17A1|80781:COL18A1|1504:CTRB1|206358:SLC36A1	Hartnup disorder|Lysinuric protein intolerance (LPI)|Cystinuria|Iminoglycinuria|Dicarboxylic aminoaciduria|Hereditary pancreatitis	Alogliptin benzoate (JAN/USAN)|Denagliptin tosylate (USAN)|Sitagliptin phosphate hydrate (JAN)|Vildagliptin (JAN/USAN/INN)|Sitagliptin (Prop.INN)|Teneligliptin (INN)|Carmegliptin (USAN/INN)|Saxagliptin (INN)|Carmegliptin dihydrochloride (USAN)|Dutogliptin (USAN)|Dutogliptin tartrate (USAN)|Linagliptin (JAN/USAN/INN)|Gosogliptin (USAN/INN)|Saxagliptin hydrate (JAN/USAN)|Teneligliptin hydrobromide hydrate (JAN)|Anagliptin (JAN/INN)	Protein is a dietary component essential for nutritional homeostasis in humans. Normally, ingested protein undergoes a complex series of degradative processes following the action of gastric, pancreatic and small intestinal enzymes. The result of this proteolytic activity is a mixture of amino acids and small peptides. Amino acids (AAs) are transported into the enterocyte (intestinal epithelial cell) by a variety of AA transporters that are specific for cationic (basic) AA, neutral AA, and anionic (acidic) AA. Small peptides are absorbed into enterocytes by the PEPT1 transporter. Inside enterocytes peptides are hydrolyzed, and the resulting amino acids are released together with those absorbed by AA transporters into blood via multiple, basolateral, AA transporters. Hydrolysis-resistant peptides, however, are transported out of the cells by a basolateral peptide transporter that has not been identified molecularly.
hsa00380	Tryptophan metabolism - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	6999:TDO2|169355:IDO2|3620:IDO1|125061:AFMID|8564:KMO|8942:KYNU|23498:HAAO|130013:ACMSD|55753:OGDHL|4967:OGDH|2639:GCDH|3030:HADHA|1962:EHHADH|1892:ECHS1|3033:HADH|38:ACAT1|39:ACAT2|883:CCBL1|56267:CCBL2|51166:AADAT|7166:TPH1|121278:TPH2|1644:DDC|4129:MAOB|4128:MAOA|219:ALDH1B1|224:ALDH3A2|217:ALDH2|501:ALDH7A1|223:ALDH9A1|316:AOX1|438:ASMT|15:AANAT|1543:CYP1A1|1544:CYP1A2|1545:CYP1B1|11185:INMT|259307:IL4I1|26:ABP1|847:CAT	Glutaric acidemia|Acatalasia|Brunner syndrome|Delayed sleep phase syndrome|Peters anomaly|Aromatic L-amino acid decarboxylase (AADC) deficiency|Primary congenital glaucoma (PCG)	Cyanamide (JP16)|Disulfiram (JP16/USP/INN)|Isoniazid (JP16/USP/INN)|Methyldopa hydrate (JP16)|Phenelzine sulfate (USP)|Carbidopa hydrate (JP16)|Selegiline hydrochloride (JAN/USP)|Tranylcypromine sulfate (USP XXI)|Lazabemide hydrochloride (JAN/USAN)|Amezinium metilsulfate (JAN)|Isoniazid calcium pyruvinate (JAN)|Benserazide hydrochloride (JP16)|Safrazine hydrochloride (JAN)|Isoniazid sodium methanesulfonate hydrate (JAN)|Toloxatone (INN)|Brofaromine (INN)|Moclobemide (USAN/INN)|Rasagiline mesylate (USAN)|Befloxatone (INN)|Pargyline hydrochloride (USAN)|Iproniazid (INN)|Isocarboxazid (INN)|Cimoxatone (INN)|Benserazide (USAN/INN)|Ladostigil tartrate (USAN)|Clorgiline (INN)|Caroxazone (USAN/INN)|Selegiline (USAN/INN)|Mofegiline hydrochloride (USAN)|Lazabemide (USAN/INN)|Milacemide hydrochloride (USAN)|Minaprine (USAN/INN)|Minaprine hydrochloride (USAN)|Nialamide (INN)|Iproclozide (INN)|Iproniazid phosphate|Methyldopa (INN)|Phenelzine (BAN)|Pargyline (INN)|Rasagiline (USAN/INN)|Tranylcypromine (INN)	
hsa00230	Purine metabolism - Homo sapiens (human)	Metabolism; Nucleotide Metabolism	53343:NUDT9|56985:C17orf48|11164:NUDT5|5236:PGM1|55276:PGM2|5634:PRPS2|5631:PRPS1|221823:PRPS1L1|5471:PPAT|2618:GART|5198:PFAS|10606:PAICS|158:ADSL|471:ATIC|353:APRT|4907:NT5E|22978:NT5C2|51251:NT5C3|56953:NT5M|30833:NT5C|93034:NT5C1B|84618:NT5C1A|4860:PNP|3251:HPRT1|3615:IMPDH2|3614:IMPDH1|8382:NME5|4832:NME3|4830:NME1|10201:NME6|4833:NME4|29922:NME7|654364:NME1-NME2|4831:NME2|377841:ENTPD8|956:ENTPD3|953:ENTPD1|124583:CANT1|9583:ENTPD4|957:ENTPD5|955:ENTPD6|3704:ITPA|7498:XDH|318:NUDT2|8833:GMPS|2766:GMPR|51292:GMPR2|9615:GDA|2987:GUK1|5315:PKM2|5313:PKLR|6240:RRM1|6241:RRM2|50484:RRM2B|1716:DGUOK|25885:POLR1A|84172:POLR1B|30834:ZNRD1|221830:TWISTNB|64425:POLR1E|5430:POLR2A|5431:POLR2B|5432:POLR2C|5433:POLR2D|5434:POLR2E|5435:POLR2F|5436:POLR2G|5437:POLR2H|5438:POLR2I|5441:POLR2L|5439:POLR2J|246721:POLR2J2|548644:POLR2J3|5440:POLR2K|11128:POLR3A|55703:POLR3B|10623:POLR3C|661:POLR3D|55718:POLR3E|9533:POLR1C|51728:POLR3K|51082:POLR1D|171568:POLR3H|10622:POLR3G|84265:POLR3GL|10621:POLR3F|5422:POLA1|23649:POLA2|5557:PRIM1|5558:PRIM2|5424:POLD1|5425:POLD2|10714:POLD3|57804:POLD4|5426:POLE|5427:POLE2|54107:POLE3|56655:POLE4|58497:PRUNE|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|55811:ADCY10|2982:GUCY1A3|2977:GUCY1A2|2983:GUCY1B3|2984:GUCY2C|3000:GUCY2D|2986:GUCY2F|4881:NPR1|4882:NPR2|5141:PDE4A|5142:PDE4B|8622:PDE8B|5143:PDE4C|5150:PDE7A|5151:PDE8A|5138:PDE2A|5144:PDE4D|10846:PDE10A|27115:PDE7B|5136:PDE1A|5137:PDE1C|5153:PDE1B|5140:PDE3B|5139:PDE3A|8654:PDE5A|5145:PDE6A|5158:PDE6B|5146:PDE6C|5147:PDE6D|5148:PDE6G|5149:PDE6H|5152:PDE9A|50940:PDE11A|159:ADSS|122622:ADSSL1|272:AMPD3|270:AMPD1|271:AMPD2|132:ADK|1633:DCK|100:ADA|204:AK2|205:AK4|26289:AK5|203:AK1|122481:AK7|954:ENTPD2|84284:NTPCR|87178:PNPT1|2272:FHIT|9060:PAPSS2|9061:PAPSS1|5169:ENPP3|5167:ENPP1|646625:PRHOXNB|55821:ALLC|100507855:adenylate|374659:HDDC3	Xanthinuria|Lesch-Nyhan syndrome|Adenine phosphoribosyltransferase deficiency|Phosphoribosylpyrophosphate synthetase I superactivity|Adenylosuccinate lyase deficiency|Mitochondrial DNA depletion syndrome (MDS)|Cone-rod dystrophy and cone dystrophy|Desbuquois syndrome|Anemia due to disorders of nucleotide metabolism|SEMD, Pakistani type|Calcification of joints and arteries|Leber congenital amaurosis (LCR)|Arts syndrome|AICA-ribosiduria|Generalized arterial calcification of infancy|Pyruvate kinase (PK) deficiency|Progressive external ophthalmoplegia (PEO)|Reticular dysgenesis	Pentostatin (JAN/USAN/INN)|Allopurinol (JP16/USP/INN)|Amrinone (JAN/INN)|Dipyridamole (JP16/USP/INN)|Hydroxycarbamide (JAN/INN)|Theophylline (JP16)|Milrinone (JAN/USP/INN)|Anhydrous caffeine (JP16)|Mycophenolate mofetil (JAN/USAN)|Pimobendan (JAN/USAN/INN)|Gemcitabine hydrochloride (JAN/USAN)|Febuxostat (JAN/USAN/INN)|Caffeine hydrate (JP16)|Vesnarinone (JAN/USAN/INN)|Colforsin daropate hydrochloride (JAN)|Theophylline sodium acetate (JAN)|Proxyphylline (JAN/INN)|Cilostazol (JP16/USAN/INN)|Tadalafil (JAN/USAN/INN)|Choline theophylline (JAN)|Olprinone hydrochloride hydrate (JAN)|Inamrinone lactate|Milrinone lactate|Papaverine hydrochloride (JP16/USP)|Sildenafil citrate (JAN/USAN)|Oxypurinol (USAN)|Gemcitabine (USAN/INN)|Vardenafil dihydrochoride (USAN)|Avanafil (USAN/INN)|Vardenafil hydrochloride hydrate (JAN)|Dasantafil (USAN/INN)|Pemetrexed disodium (USAN)|Enoximone (USAN/INN)|Filaminast (USAN/INN)|Forodesine hydrochloride (JAN/USAN)|Imazodan hydrochloride (USAN)|Indolidan (USAN/INN)|Isomazole hydrochloride (USAN)|Levosimendan (USAN/INN)|Lixazinone sulfate (USAN)|Merimepodib (USAN/INN)|Mycophenolate mofetil hydrochloride (USAN)|Mycophenolate sodium (USAN)|Pelitrexol (USAN/INN)|Aminophylline hydrate (JP16)|Piclamilast (USAN/INN)|Roflumilast (JAN/USAN/INN)|Theophylline (USP)|Theophylline sodium glycinate (USP)|Pemetrexed sodium hydrate (JAN)|Forodesine (USAN/INN)|Pemetrexed (INN)|Allopurinol sodium|Flavoxate (INN)|Sildenafil (INN)|Vardenafil (INN)|Vardenafil hydrochloride (USAN)|Udenafil (USAN/INN)	
hsa04520	Adherens junction - Homo sapiens (human)	Cellular Processes; Cell Communication	5818:PVRL1|5819:PVRL2|25945:PVRL3|81607:PVRL4|56288:PARD3|6714:SRC|9855:FARP2|998:CDC42|5879:RAC1|5880:RAC2|5881:RAC3|7454:WAS|8976:WASL|10458:BAIAP2|8936:WASF1|10163:WASF2|10810:WASF3|4301:MLLT4|4008:LMO7|117178:SSX2IP|10580:SORBS1|81:ACTN4|88:ACTN2|87:ACTN1|89:ACTN3|7414:VCL|7082:TJP1|999:CDH1|1500:CTNND1|1499:CTNNB1|1496:CTNNA2|1495:CTNNA1|29119:CTNNA3|60:ACTB|71:ACTG1|387:RHOA|5797:PTPRM|5787:PTPRB|5792:PTPRF|5770:PTPN1|5777:PTPN6|5795:PTPRJ|1459:CSNK2A2|1457:CSNK2A1|1460:CSNK2B|6932:TCF7|83439:TCF7L1|6934:TCF7L2|51176:LEF1|3480:IGF1R|3643:INSR|4233:MET|1956:EGFR|2064:ERBB2|2260:FGFR1|2534:FYN|7525:YES1|5594:MAPK1|5595:MAPK3|6591:SNAI2|6615:SNAI1|7046:TGFBR1|7048:TGFBR2|4087:SMAD2|4088:SMAD3|4089:SMAD4|1387:CREBBP|2033:EP300|6885:MAP3K7|51701:NLK|2241:FER|52:ACP1|8826:IQGAP1	Piebaldism|Nephrotic syndrome and focal segmental glomerulosclerosis|Ectodermal dysplasia-syndactyly syndrome (EDSS)|Leprechaunism |Waardenburg syndrome (WS)|Loeys-Dietz syndrome (LDS)|Familial thoracic aortic aneurysm and dissection (TAAD)|Rabson-Mendenhall syndrome|Pilomatricoma|Juvenile polyposis syndrome|Trigonocephaly	Insulin (JAN/USP)|Mecasermin (genetical recombination) (JAN)|Insulin human, isophane (USP)|Insulin human zinc (USP)|Insulin human zinc, extended (USP)|Insulin I 125 (USAN)|Insulin I 131 (USAN)|Insulin, dalanated (USAN)|Isophane insulin injection (aqueous suspension) (JAN)|Insulin, neutral (USAN)|Insulin zinc, extended (USP)|Insulin zinc, prompt (USP)|Insulin zinc (USP)|Mecasermin rinfabate (USAN/INN)|Proinsulin human (USAN)|Insulin injection, biphasic isophane (BAN)|Insulin degludec (genetical recombination) (JAN)	Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue architecture and cell polarity and can limit cell movement and proliferation. At AJs, E-cadherin serves as an essential cell adhesion molecules (CAMs). The cytoplasmic tail binds beta-catenin, which in turn binds alpha-catenin. Alpha-catenin is associated with F-actin bundles directly and indirectly. The integrity of the cadherin-catenin complex is negatively regulated by phosphorylation of beta-catenin by receptor tyrosine kinases (RTKs) and cytoplasmic tyrosine kinases (Fer, Fyn, Yes, and Src), which leads to dissociation of the cadherin-catenin complex. Integrity of this complex is positively regulated by beta -catenin phosphorylation by casein kinase II, and dephosphorylation by protein tyrosine phosphatases. Changes in the phosphorylation state of beta-catenin affect cell-cell adhesion, cell migration and the level of signaling beta-catenin. Wnt signaling acts as a positive regulator of beta-catenin by inhibiting beta-catenin degradation, which stabilizes beta-catenin, and causes its accumulation. Cadherin may acts as a negative regulator of signaling beta-catenin as it binds beta-catenin at the cell surface and thereby sequesters it from the nucleus. Nectins also function as CAMs at AJs, but are more highly concentrated at AJs than E-cadherin. Nectins transduce signals through Cdc42 and Rac, which reorganize the actin cytoskeleton, regulate the formation of AJs, and strengthen cell-cell adhesion.
hsa05213	Endometrial cancer - Homo sapiens (human)	Human Diseases; Cancers	1950:EGF|1956:EGFR|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5728:PTEN|5170:PDPK1|3611:ILK|207:AKT1|208:AKT2|10000:AKT3|842:CASP9|572:BAD|2309:FOXO3|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|2002:ELK1|4292:MLH1|999:CDH1|1499:CTNNB1|1496:CTNNA2|1495:CTNNA1|29119:CTNNA3|8312:AXIN1|8313:AXIN2|10297:APC2|324:APC|2932:GSK3B|6932:TCF7|83439:TCF7L1|6934:TCF7L2|51176:LEF1|4609:MYC|595:CCND1|7157:TP53|2064:ERBB2	Endometrial Cancer|Mismatch repair deficiency		Endometrial cancer (EC) is the most common gynaecological malignancy and the fourth most common malignancy in women in the developed world after breast, colorectal and lung cancer. Two types of endometrial carcinoma are distinguished with respect to biology and clinical course. Type-I carcinoma is related to hyperestrogenism by association with endometrial hyperplasia, frequent expression of estrogen and progesterone receptors and younger age, whereas type-II carcinoma is unrelated to estrogen, associated with atrophic endometrium, frequent lack of estrogen and progesterone receptors and older age. The morphologic differences in these cancers are mirrored in their molecular genetic profile with type I showing defects in DNA-mismatch repair and mutations in PTEN, K-ras, and beta-catenin, and type II showing aneuploidy, p53 mutations, and her2/neu amplification.
hsa05168	Herpes simplex infection - Homo sapiens (human)	Human Diseases; Infectious Diseases	4049:LTA|8740:TNFSF14|8764:TNFRSF14|7185:TRAF1|7186:TRAF2|7187:TRAF3|7188:TRAF5|5602:MAPK10|5601:MAPK9|5599:MAPK8|3725:JUN|2353:FOS|8517:IKBKG|4792:NFKBIA|4793:NFKBIB|4790:NFKB1|5970:RELA|5818:PVRL1|5819:PVRL2|29992:PILRA|5781:PTPN11|7097:TLR2|4615:MYD88|7189:TRAF6|10454:TAB1|23118:TAB2|6885:MAP3K7|54106:TLR9|7098:TLR3|148022:TICAM1|3661:IRF3|3665:IRF7|23586:DDX58|64135:IFIH1|57506:MAVS|9641:IKBKE|29110:TBK1|6347:CCL2|6352:CCL5|7124:TNF|3553:IL1B|3569:IL6|3592:IL12A|3593:IL12B|3600:IL15|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3434:IFIT1|439996:IFIT1B|7874:USP7|5610:EIF2AK2|27102:EIF2AK1|440275:EIF2AK4|9451:EIF2AK3|1965:EIF2S1|5501:PPP1CC|5499:PPP1CA|5500:PPP1CB|4938:OAS1|4940:OAS3|4939:OAS2|6041:RNASEL|718:C3|727:C5|5199:CFP|6500:SKP1|997:CDC34|54926:UBE2R2|8454:CUL1|6502:SKP2|1936:EEF1D|29997:GLTSCR2|10445:MCRS1|5430:POLR2A|6732:SRPK1|8683:SRSF9|6426:SRSF1|6427:SRSF2|10929:SRSF8|6428:SRSF3|6430:SRSF5|6429:SRSF4|6431:SRSF6|6432:SRSF7|5371:PML|6672:SP100|1387:CREBBP|2033:EP300|7157:TP53|1616:DAXX|983:CDK1|1017:CDK2|1459:CSNK2A2|1457:CSNK2A1|1460:CSNK2B|3054:HCFC1|29915:HCFC2|387332:TBPL2|9519:TBPL1|6908:TBP|51616:TAF9B|6878:TAF6|10629:TAF6L|6877:TAF5|27097:TAF5L|6874:TAF4|6875:TAF4B|83860:TAF3|6884:TAF13|6881:TAF10|112950:MED8|9569:GTF2IRD1|2969:GTF2I|3150:HMGN1|10189:ALYREF|55998:NXF5|56000:NXF3|56001:NXF2|10482:NXF1|728343:NXF2B|708:C1QBP|3190:HNRNPK|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|972:CD74|6890:TAP1|6891:TAP2|3133:HLA-E|3134:HLA-F|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|3456:IFNB1|3454:IFNAR1|3455:IFNAR2|3716:JAK1|7297:TYK2|6772:STAT1|6773:STAT2|10379:IRF9|9021:SOCS3|3458:IFNG|3459:IFNGR1|3460:IFNGR2|3717:JAK2|356:FASLG|355:FAS|7132:TNFRSF1A|8772:FADD|841:CASP8|836:CASP3|54205:CYCS|406:ARNTL|9575:CLOCK|8863:PER3|8864:PER2|5187:PER1|25833:POU2F3			Herpes simplex virus (HSV) infections are very common worldwide, with the prevalence of HSV-1 reaching up to 80%-90%. Primary infection with HSV takes place in the mucosa, followed by the establishment of latent infection in neuronal ganglia. HSV is the main cause of herpes infections that lead to the formation of characteristic blistering lesion. HSV express multiple viral accessory proteins that interfere with host immune responses and are indispensable for viral replication. Among these proteins, the immediate early (IE) gene ICP0, ICP4, and ICP27 are essential for regulation of HSV gene expression in productive infection. On the other hand, ORF P and ORF O gene are transcribed during latency and blocks the expression of the IE genes, thus maintaining latent infection.
hsa04720	Long-term potentiation - Homo sapiens (human)	Organismal Systems; Nervous System	2890:GRIA1|2891:GRIA2|107:ADCY1|114:ADCY8|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|5502:PPP1R1A|5501:PPP1CC|5499:PPP1CA|5500:PPP1CB|4659:PPP1R12A|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|10411:RAPGEF3|5906:RAP1A|5908:RAP1B|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|2902:GRIN1|2903:GRIN2A|2904:GRIN2B|2905:GRIN2C|2906:GRIN2D|775:CACNA1C|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|1387:CREBBP|2033:EP300|468:ATF4|814:CAMK4|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|6195:RPS6KA1|6196:RPS6KA2|6197:RPS6KA3|27330:RPS6KA6|3708:ITPR1|3709:ITPR2|3710:ITPR3|5579:PRKCB|5578:PRKCA|5582:PRKCG|2911:GRM1|2915:GRM5|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1		Topiramate (JAN/USAN/INN)|Amantadine hydrochloride (JP16/USP)|Dextromethorphan hydrobromide hydrate (JP16)|Ifenprodil tartrate (JP16)|Selfotel (USAN/INN)|Talampanel (INN)|Aptiganel hydrochloride (USAN)|Besonprodil (USAN)|Delucemine hydrochloride (USAN)|Dextromethorphan (USP)|Dextromethorphan polistirex (USAN)|Dextrorphan hydrochloride (USAN)|Dizocilpine maleate (USAN)|Fenobam (USAN)|Flupirtine maleate (USAN)|Gavestinel (USAN/INN)|Licostinel (USAN/INN)|Memantine hydrochloride (JAN/USAN)|Neramexane mesylate (USAN)|Perzinfotel (USAN/INN)|Phencyclidine hydrochloride (USAN)|Remacemide hydrochloride (USAN)|Traxoprodil mesylate (USAN)|Esketamine (INN)|Amantadine (INN)|Ifenprodil (INN)|Levomethadone (INN)|Levomethadone hydrochloride|Memantine (INN)|Methadone (BAN)	Hippocampal long-term potentiation (LTP), a long-lasting increase in synaptic efficacy, is the molecular basis for learning and memory. Tetanic stimulation of afferents in the CA1 region of the hippocampus induces glutamate release and activation of glutamate receptors in dendritic spines. A large increase in [Ca2+]i resulting from influx through NMDA receptors leads to constitutive activation of CaM kinase II (CaM KII) . Constitutively active CaM kinase II phosphorylates AMPA receptors, resulting in potentiation of the ionic conductance of AMPA receptors. Early-phase LTP (E-LTP) expression is due, in part, to this phosphorylation of the AMPA receptor. It is hypothesized that postsynaptic Ca2+ increases generated through NMDA receptors activate several signal transduction pathways including the Erk/MAP kinase and cAMP regulatory pathways. The convergence of these pathways at the level of the CREB/CRE transcriptional pathway may increase expression of a family of genes required for late-phase LTP (L-LTP).
hsa00512	Mucin type O-Glycan biosynthesis - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	168391:GALNTL5|2591:GALNT3|8693:GALNT4|2589:GALNT1|57452:GALNTL1|55568:GALNT10|11227:GALNT5|26290:GALNT8|11226:GALNT6|51809:GALNT7|50614:GALNT9|63917:GALNT11|79695:GALNT12|79623:GALNT14|114805:GALNT13|117248:GALNTL2|64409:WBSCR17|374378:GALNTL4|2590:GALNT2|442117:GALNTL6|56913:C1GALT1|29071:C1GALT1C1|2650:GCNT1|9245:GCNT3|51301:GCNT4|6482:ST3GAL1|6483:ST3GAL2|55808:ST6GALNAC1|192134:B3GNT6|9334:B4GALT5|100528030:POC1B-GALNT4	Tn syndrome|Familial tumoral calcinosis (FTC)		O-glycans are a class of glycans that modify serine or threonine residues of proteins. Biosynthesis of O-glycans starts from the transfer of N-acetylgalactosamine (GalNAc) to serine or threonine. The first GalNAc may be extended with sugars including galactose, N-acetylglucosamine, fucose, or sialic acid, but not mannose, glucose, or xylose. Depending on the sugars added, there are four common O-glycan core structures, cores 1 through 4, and an additional four, cores 5 though 8. Mucins are highly O-glycosylated glycoproteins ubiquitous in mucous secretions on cell surfaces and in body fluids. Mucin O-glycans can be branched, and many sugars or groups of sugars are antigenic. Important modifications of mucin O-glycans include O-acetylation of sialic acid and O-sulfation of galactose and N-acetylglucosamine.
hsa05143	African trypanosomiasis - Homo sapiens (human)	Human Diseases; Infectious Diseases	100132941:uncharacterized|100291917:uncharacterized|54106:TLR9|4615:MYD88|7064:THOP1|335:APOA1|3250:HPR|3039:HBA1|3040:HBA2|3045:HBD|3043:HBB|3586:IL10|3592:IL12A|3593:IL12B|3606:IL18|3458:IFNG|7124:TNF|3553:IL1B|3569:IL6|356:FASLG|355:FAS|7412:VCAM1|6401:SELE|3383:ICAM1|3910:LAMA4|169355:IDO2|3620:IDO1|2150:F2RL1|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|5579:PRKCB|5578:PRKCA|5582:PRKCG|8542:APOL1	African trypanosomiasis		Trypanosoma brucei, the parasite responsible for African trypanosomiasis (sleeping sickness), are spread by the tsetse fly in sub-Saharan Africa. The parasites are able to pass through the blood-brain barrier and cause neurological damage by inducing cytokines like TNF alpha, IFN gamma, and IL1. These cytokines and other metabolites such as nitric oxide and somnogenic prostaglandin D2 disturb circadian rhythms in patients with African trypanosomiasis.
hsa04144	Endocytosis - Homo sapiens (human)	Cellular Processes; Transport and Catabolism	7040:TGFB1|7042:TGFB2|7043:TGFB3|7046:TGFBR1|7048:TGFBR2|9765:ZFYVE16|9372:ZFYVE9|5371:PML|4087:SMAD2|4088:SMAD3|7037:TFRC|1956:EGFR|2321:FLT1|3791:KDR|5156:PDGFRA|2263:FGFR2|2261:FGFR3|2264:FGFR4|3480:IGF1R|4233:MET|4914:NTRK1|2065:ERBB3|2066:ERBB4|3815:KIT|5979:RET|1436:CSF1R|1950:EGF|26052:DNM3|1785:DNM2|10059:DNM1L|1759:DNM1|382:ARF6|8394:PIP5K1A|8395:PIP5K1B|23396:PIP5K1C|138429:PIP5KL1|5337:PLD1|5338:PLD2|1211:CLTA|1212:CLTB|8218:CLTCL1|1213:CLTC|161:AP2A2|160:AP2A1|163:AP2B1|1173:AP2M1|1175:AP2S1|30846:EHD2|23624:CBLC|868:CBLB|867:CBL|4734:NEDD4|23327:NEDD4L|4193:MDM2|7189:TRAF6|10193:RNF41|83737:ITCH|57154:SMURF1|64750:SMURF2|11059:WWP1|30011:SH3KBP1|6457:SH3GL3|6456:SH3GL2|6455:SH3GL1|56904:SH3GLB2|51100:SH3GLB1|22905:EPN2|29924:EPN1|55040:EPN3|2060:EPS15|3949:LDLR|26119:LDLRAP1|1601:DAB2|1234:CCR5|3577:CXCR1|3579:CXCR2|7852:CXCR4|2149:F2R|153:ADRB1|154:ADRB2|155:ADRB3|6011:GRK1|131890:GRK7|156:ADRBK1|157:ADRBK2|2868:GRK4|2869:GRK5|2870:GRK6|409:ARRB2|408:ARRB1|4091:SMAD6|4092:SMAD7|390243:FOLR4|2352:FOLR3|2350:FOLR2|2348:FOLR1|857:CAV1|858:CAV2|859:CAV3|3133:HLA-E|3134:HLA-F|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|3559:IL2RA|3560:IL2RB|3561:IL2RG|6714:SRC|3265:HRAS|387:RHOA|3306:HSPA2|3310:HSPA6|3304:HSPA1B|3305:HSPA1L|3312:HSPA8|3303:HSPA1A|9829:DNAJC6|9101:USP8|10617:STAMBP|7879:RAB7A|9146:HGS|10254:STAM2|8027:STAM|7251:TSG101|93343:FAM125A|89853:FAM125B|51160:VPS28|55048:VPS37C|155382:VPS37D|137492:VPS37A|79720:VPS37B|11267:SNF8|51028:VPS36|84313:VPS25|79643:CHMP6|29082:CHMP4A|92421:CHMP4C|128866:CHMP4B|51652:CHMP3|27243:CHMP2A|25978:CHMP2B|91782:CHMP7|9525:VPS4B|27183:VPS4A|51534:VTA1|57132:CHMP1B|51510:CHMP5|10015:PDCD6IP|30845:EHD3|30844:EHD4|8411:EEA1|5868:RAB5A|5869:RAB5B|5878:RAB5C|11311:VPS45|9135:RABEP1|64145:ZFYVE20|5867:RAB4A|80230:RUFY1|10938:EHD1|8766:RAB11A|9230:RAB11B|26056:RAB11FIP5|22841:RAB11FIP2|80223:RAB11FIP1|9727:RAB11FIP3|84440:RAB11FIP4|57403:RAB22A|11031:RAB31|56288:PARD3|50855:PARD6A|84552:PARD6G|84612:PARD6B|5584:PRKCI|5590:PRKCZ|998:CDC42|64744:SMAP2|60682:SMAP1|28964:GIT1|9815:GIT2|50807:ASAP1|8853:ASAP2|55616:ASAP3|9744:ACAP1|23527:ACAP2|116983:ACAP3|116985:ARAP1|116984:ARAP2|64411:ARAP3|116987:AGAP1|116986:AGAP2|55738:ARFGAP1|26286:ARFGAP3|84364:ARFGAP2|5662:PSD|23362:PSD3|23550:PSD4|84249:PSD2|9922:IQSEC1|23096:IQSEC2|440073:IQSEC3	Frontotemporal lobar degeneration (FTLD)|Hypercholesterolemia, autosomal dominant|Caveolinopathies|Limb-girdle muscular dystrophy (LGMD)|Lacrimo-auriculo-dento-digital syndrome (LADD)|Centronuclear myopathy|Loeys-Dietz syndrome (LDS)|Lethal congenital contractural syndrome (LCCS)	Adrenaline (JP16)|Betaxolol hydrochloride (JP16/USP)|Carteolol hydrochloride (JP16/USP)|Timolol maleate (JP16/USP)|Salbutamol sulfate (JP16)|Bitolterol mesilate (JAN)|Orciprenaline sulfate (JP16)|Pirbuterol acetate (USAN)|Salmeterol xinafoate (JAN/USAN)|Terbutaline sulfate (JP16/USP)|Levobunolol hydrochloride (JAN/USP)|Pirbuterol hydrochloride (JAN/USAN)|Clenbuterol hydrochloride (JAN/USP)|Tulobuterol hydrochloride (JP16)|Formoterol fumarate (USAN)|Fenoterol hydrobromide (JAN)|Mabuterol hydrochloride (JAN)|Methoxyphenamine hydrochloride (JAN)|Nipradilol (JAN/INN)|Isoxsuprine hydrochloride (JP16/USP)|Trimetoquinol hydrochloride|Isoetharine hydrochloride (USP)|Albuterol (USP)|Tulobuterol (JAN/INN)|Levalbuterol hydrochloride (USAN)|Hexoprenaline sulfate (USAN)|Procaterol hydrochloride (USAN)|Arformoterol tartrate (USAN)|Basiliximab (genetical recombination) (JAN)|Butoxamine hydrochloride (USAN)|Mecasermin (genetical recombination) (JAN)|Carbuterol hydrochloride (USAN)|Colterol mesylate (USAN)|Daclizumab (USAN/INN)|Denileukin diftitox (USAN/INN)|Dopexamine (USAN/INN)|Fenoterol (USAN/INN)|Isoetharine (USP)|Isoetharine mesylate (USP)|Levalbuterol tartrate (USAN)|Levobetaxolol hydrochloride (USAN)|Mecasermin rinfabate (USAN/INN)|Metaproterenol polistirex (USAN)|Trimetoquinol hydrochloride hydrate (JP16)|Formoterol fumarate hydrate (JP16)|Procaterol hydrochloride hydrate (JP16)|Picumeterol fumarate (USAN)|Reproterol hydrochloride (USAN)|Rimiterol hydrobromide (USAN)|Salmeterol (USAN/INN)|Sibenadet hydrochloride (USAN)|Solabegron hydrochloride (USAN)|Vicriviroc maleate (USAN)|Aplaviroc hydrochloride (USAN)|Maraviroc (JAN/INN)|Bambuterol (INN)|Arformoterol (INN)|Bambuterol hydrocloride|Betaxolol (INN)|Bitolterol (INN)|Carazolol (INN)|Carteolol (INN)|Clenbuterol (INN)|Formoterol (INN)|Hexoprenaline (INN)|Isoxsuprine (INN)|Isoxsuprine lactate|Levobunolol (INN)|Levosalbutamol (INN)|Orciprenaline (INN)|Pirbuterol (INN)|Procaterol (INN)|Reproterol (INN)|Terbutaline (INN)|Tretoquinol (INN)|Indacaterol (USAN/INN)|Indacaterol maleate (JAN/USAN)|Mirabegron (USAN/JAN)|Bosutinib hydrate (JAN)|Ritobegron ethyl hydrochloride (JAN)|Olodaterol hydrochloride (JAN/USAN)	Endocytosis is a mechanism for cells to remove ligands, nutrients, and plasma membrane (PM) proteins, and lipids from the cell surface, bringing them into the cell interior. Transmembrane proteins entering through clathrin-dependent endocytosis (CDE) have sequences in their cytoplasmic domains that bind to the APs (adaptor-related protein complexes) and enable their rapid removal from the PM. In addition to APs and clathrin, there are numerous accessory proteins including dynamin. Depending on the various proteins that enter the endosome membrane, these cargoes are sorted to distinct destinations. Some cargoes, such as nutrient receptors, are recycled back to the PM. Ubiquitylated membrane proteins, such as activated growth-factor receptors, are sorted into intraluminal vesicles and eventually end up in the lysosome lumen via multivesicular endosomes (MVEs). There are distinct mechanisms of clathrin-independent endocytosis (CIE) depending upon the cargo and the cell type.
hsa03020	RNA polymerase - Homo sapiens (human)	Genetic Information Processing; Transcription	5431:POLR2B|5430:POLR2A|5432:POLR2C|5439:POLR2J|246721:POLR2J2|548644:POLR2J3|5433:POLR2D|5436:POLR2G|5438:POLR2I|5434:POLR2E|5435:POLR2F|5437:POLR2H|5440:POLR2K|5441:POLR2L|55703:POLR3B|11128:POLR3A|51082:POLR1D|9533:POLR1C|10623:POLR3C|661:POLR3D|55718:POLR3E|51728:POLR3K|171568:POLR3H|10622:POLR3G|84265:POLR3GL|10621:POLR3F|84172:POLR1B|25885:POLR1A|30834:ZNRD1|64425:POLR1E|221830:TWISTNB	Treacher Collins syndrome		
hsa04670	Leukocyte transendothelial migration - Homo sapiens (human)	Organismal Systems; Immune System	83700:JAM3|3684:ITGAM|3689:ITGB2|58494:JAM2|3676:ITGA4|3688:ITGB1|5175:PECAM1|4267:CD99|3683:ITGAL|50848:F11R|1003:CDH5|9080:CLDN9|7122:CLDN5|9071:CLDN10|9075:CLDN2|1365:CLDN3|9074:CLDN6|9073:CLDN8|5010:CLDN11|23562:CLDN14|9076:CLDN1|24146:CLDN15|26285:CLDN17|53842:CLDN22|10686:CLDN16|49861:CLDN20|149461:CLDN19|137075:CLDN23|1366:CLDN7|1364:CLDN4|51208:CLDN18|100506658:OCLN|90952:ESAM|7412:VCAM1|7430:EZR|4478:MSN|60:ACTB|71:ACTG1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5879:RAC1|50508:NOX3|1536:CYBB|27035:NOX1|1535:CYBA|4688:NCF2|653361:NCF1|4689:NCF4|1499:CTNNB1|1500:CTNND1|1496:CTNNA2|1495:CTNNA1|29119:CTNNA3|5781:PTPN11|4313:MMP2|4318:MMP9|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|3383:ICAM1|5335:PLCG1|5336:PLCG2|5579:PRKCB|5578:PRKCA|5582:PRKCG|5747:PTK2|5829:PXN|9564:BCAR1|7070:THY1|2909:ARHGAP35|394:ARHGAP5|387:RHOA|6093:ROCK1|9475:ROCK2|4633:MYL2|4636:MYL5|58498:MYL7|10398:MYL9|93408:MYL10|10627:MYL12A|103910:MYL12B|29895:MYLPF|4301:MLLT4|5906:RAP1A|5908:RAP1B|6494:SIPA1|7408:VASP|81:ACTN4|88:ACTN2|87:ACTN1|89:ACTN3|7414:VCL|6387:CXCL12|7852:CXCR4|2773:GNAI3|2770:GNAI1|2771:GNAI2|10411:RAPGEF3|11069:RAPGEF4|83593:RASSF5|2185:PTK2B|3702:ITK|7294:TXK|10451:VAV3|7409:VAV1|7410:VAV2|5880:RAC2|998:CDC42|399:RHOH	Leukocyte adhesion deficiency (LAD)|Neonatal ichthyosis-sclerosing cholangitis (NISCH) syndrome|Band-like calcification with simplified gyration and polymicrogyria (BLC-PMG)|Pilomatricoma|Metachondromatosis	Procaterol hydrochloride (USAN)|Alicaforsen sodium (USAN)|Batimastat (USAN/INN)|Efalizumab (USAN/INN)|Valategrast hydrochloride (USAN)	Leukocyte migaration from the blood into tissues is vital for immune surveillance and inflammation. During this diapedesis of leukocytes, the leukocytes bind to endothelial cell adhesion molecules (CAM) and then migrate across the vascular endothelium. A leukocyte adherent to CAMs on the endothelial cells moves forward by leading-edge protrusion and retraction of its tail. In this process, alphaL /beta2 integrin activates through Vav1, RhoA, which subsequently activates the kinase p160ROCK. ROCK activation leads to MLC phosphorylation, resulting in retraction of the actin cytoskeleton. Moreover, Leukocytes activate endothelial cell signals that stimulate endothelial cell retraction during localized dissociation of the endothelial cell junctions. ICAM-1-mediated signals activate an endothelial cell calcium flux and PKC, which are required for ICAM-1 dependent leukocyte migration. VCAM-1 is involved in the opening of the "endothelial passage" through which leukocytes can extravasate. In this regard, VCAM-1 ligation induces NADPH oxidase activation and the production of reactive oxygen species (ROS) in a Rac-mediated manner, with subsequent activation of matrix metallopoteinases and loss of VE-cadherin-mediated adhesion.
hsa03060	Protein export - Homo sapiens (human)	Genetic Information Processing; Folding, Sorting and Degradation	5018:OXA1L|6729:SRP54|55176:SEC61A2|29927:SEC61A1|10952:SEC61B|23480:SEC61G|7095:SEC62|11231:SEC63|3309:HSPA5|6726:SRP9|6727:SRP14|6731:SRP72|6730:SRP68|6728:SRP19|6734:SRPR|58477:SRPRB|28972:SPCS1|9789:SPCS2|60559:SPCS3|23478:SEC11A|90701:SEC11C|196294:IMMP1L|83943:IMMP2L			The protein export is the active transport of proteins from the cytoplasm to the exterior of the cell, or to the periplasmic compartment in Gram-negative bacteria. The sec dependent pathway is the general protein export system that transports newly synthesized proteins into or across the cell membrane. The translocation channel is formed from a conserved trimeric membrane protein complex, called the Sec61/SecY complex. The twin-arginine translocation (Tat) pathway is another protein transport system that transports folded proteins in bacteria, archaea, and chloroplasts. Many Tat systems comprise three functionally different membrane proteins, TatA, TatB, and TatC, but TatA and TatE seem to have overlapping functions, with TatA having by far the more important role.
hsa00830	Retinol metabolism - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	53630:BCMO1|126:ADH1C|131:ADH7|124:ADH1A|125:ADH1B|127:ADH4|128:ADH5|130:ADH6|9249:DHRS3|10901:DHRS4|317749:DHRS4L2|10170:DHRS9|50700:RDH8|157506:RDH10|51109:RDH11|145226:RDH12|8608:RDH16|8630:HSD17B6|9227:LRAT|8694:DGAT1|158835:AWAT2|8228:PNPLA4|6121:RPE65|5959:RDH5|8854:ALDH1A2|216:ALDH1A1|1592:CYP26A1|56603:CYP26B1|340665:CYP26C1|1543:CYP1A1|1544:CYP1A2|1549:CYP2A7|1548:CYP2A6|1553:CYP2A13|1555:CYP2B6|1562:CYP2C18|1559:CYP2C9|1557:CYP2C19|1558:CYP2C8|1551:CYP3A7|1577:CYP3A5|64816:CYP3A43|1576:CYP3A4|1579:CYP4A11|284541:CYP4A22|7363:UGT2B4|574537:UGT2A2|7367:UGT2B17|7365:UGT2B10|7364:UGT2B7|7366:UGT2B15|54577:UGT1A7|10720:UGT2B11|54490:UGT2B28|54579:UGT1A5|54659:UGT1A3|54657:UGT1A4|54578:UGT1A6|54576:UGT1A8|54600:UGT1A9|10941:UGT2A1|54575:UGT1A10|79799:UGT2A3|54658:UGT1A1|54884:RETSAT|195814:SDR16C5	Retinitis pigmentosa (RP)|Familial flecked retina syndrome|Leber congenital amaurosis (LCR)	Fomepizole (USAN/INN)	
hsa00250	Alanine, aspartate and glutamate metabolism - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	2805:GOT1|2806:GOT2|259307:IL4I1|8528:DDO|440:ASNS|56954:NIT2|84706:GPT2|2875:GPT|189:AGXT|64902:AGXT2|445:ASS1|435:ASL|159:ADSS|122622:ADSSL1|158:ADSL|443:ASPA|91703:ACY3|2571:GAD1|2572:GAD2|18:ABAT|7915:ALDH5A1|2746:GLUD1|2747:GLUD2|8659:ALDH4A1|2752:GLUL|790:CAD|2744:GLS|27165:GLS2|1373:CPS1|9945:GFPT2|2673:GFPT1|5471:PPAT	Canavan disease (CD)|Citrullinemia (CTLN)|Adenylosuccinate lyase deficiency|Succinic semialdehyde dehydrogenase (SSADH) deficiency|Congenital systemic glutamine deficiency (CSGD)|Argininosuccinic aciduria (ARGINSA)|Cerebral palsy	Valproic acid (USP)|Vigabatrin (JAN/USAN/INN)|Sodium valproate (JP16)|Calcium valproate	
hsa04960	Aldosterone-regulated sodium reabsorption - Homo sapiens (human)	Organismal Systems; Excretory System	3291:HSD11B2|4306:NR3C2|6337:SCNN1A|6338:SCNN1B|6340:SCNN1G|6446:SGK1|3758:KCNJ1|9351:SLC9A3R2|23327:NEDD4L|2810:SFN|3845:KRAS|476:ATP1A1|480:ATP1A4|478:ATP1A3|477:ATP1A2|481:ATP1B1|482:ATP1B2|483:ATP1B3|23439:ATP1B4|486:FXYD2|53828:FXYD4|3630:INS|3479:IGF1|3643:INSR|8471:IRS4|8660:IRS2|3667:IRS1|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|5170:PDPK1|5579:PRKCB|5578:PRKCA|5582:PRKCG|5594:MAPK1|5595:MAPK3	Bartter syndrome|Liddle syndrome|Hyperkalemic distal renal tubular acidosis (RTA type 4)|Hypertension exacerbated in pregnancy|Leprechaunism |Bronchiectasis with or without elevated sweat chloride|Rabson-Mendenhall syndrome|Alternating hemiplegia of childhood	Insulin (JAN/USP)|Triamterene (JP16/USP/INN)|Spironolactone (JP16/USP/INN)|Eplerenone (JAN/USAN/INN)|Deslanoside (JP16/USP/INN)|Proscillaridin (JAN/USAN/INN)|Potassium canrenoate (JP16)|Lanatoside C (JP16/INN)|Metildigoxin (JP16)|Insulin glargine (genetical recombination) (JAN)|Canrenone (USAN)|Desoxycorticosterone acetate (USP)|Desoxycorticosterone pivalate (USP)|Dicirenone (USAN)|Drospirenone (JAN/USP/INN)|Insulin aspart (genetical recombination) (JAN)|Insulin lispro (genetical recombination) (JAN)|Insulin glulisine (genetical recombination) (JAN)|Insulin human, isophane (USP)|Insulin human zinc (USP)|Insulin human zinc, extended (USP)|Insulin I 125 (USAN)|Insulin I 131 (USAN)|Insulin, dalanated (USAN)|Isophane insulin injection (aqueous suspension) (JAN)|Insulin, neutral (USAN)|Insulin zinc, extended (USP)|Insulin zinc, prompt (USP)|Insulin zinc (USP)|Mexrenoate potassium (USAN)|Proinsulin human (USAN)|Prorenoate potassium (USAN/INN)|Acetyldigitoxin (INN)|Gitoformate (INN)|Acetyldigoxin|Carbenoxolone (INN)|Desoxycortone (INN)|Insulin injection, biphasic isophane (BAN)|Insulin degludec (genetical recombination) (JAN)	Sodium transport across the tight epithelia of Na+ reabsorbing tissues such as the distal part of the kidney nephron and colon is the major factor determining total-body Na+ levels, and thus, long-term blood pressure. Aldosterone plays a major role in sodium and potassium metabolism by binding to epithelial mineralocorticoid receptors (MR) in the renal collecting duct cells localized in the distal nephron, promoting sodium resorption and potassium excretion. Aldosterone enters a target cell and binds MR, which translocates into the nucleus and regulates gene transcription. Activation of MR leads to increased expression of Sgk-1, which phosphorylates Nedd4-2, an ubiquitin-ligase which targets ENAC to proteosomal degradation. Phosphorylated Nedd4-2 dissociates from ENAC, increasing its apical membrane abundance. Activation of MR also leads to increased expression of Na+/K+-ATPase, thus causing a net increase in sodium uptake from the renal filtrate. The specificity of MR for aldosterone is provided by 11beta-HSD2 by the rapid conversion of cortisol to cortisone in renal cortical collecting duct cells. Recently, besides genomic effects mediated by activated MR, rapid aldosterone actions that are independent of translation and transcription have been documented.
hsa05323	Rheumatoid arthritis - Homo sapiens (human)	Human Diseases; Immune Diseases	941:CD80|942:CD86|940:CD28|1493:CTLA4|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|3683:ITGAL|3689:ITGB2|3383:ICAM1|3600:IL15|8741:TNFSF13|10673:TNFSF13B|100132941:uncharacterized|100291917:uncharacterized|4050:LTB|7124:TNF|3552:IL1A|3553:IL1B|3569:IL6|3589:IL11|3606:IL18|7097:TLR2|7099:TLR4|3725:JUN|2353:FOS|7040:TGFB1|7042:TGFB2|7043:TGFB3|51561:IL23A|3605:IL17A|1435:CSF1|8600:TNFSF11|8792:TNFRSF11A|523:ATP6V1A|526:ATP6V1B2|525:ATP6V1B1|528:ATP6V1C1|245973:ATP6V1C2|51382:ATP6V1D|529:ATP6V1E1|90423:ATP6V1E2|9296:ATP6V1F|9550:ATP6V1G1|534:ATP6V1G2|127124:ATP6V1G3|8992:ATP6V0E1|155066:ATP6V0E2|535:ATP6V0A1|50617:ATP6V0A4|23545:ATP6V0A2|10312:TCIRG1|9114:ATP6V0D1|245972:ATP6V0D2|51606:ATP6V1H|537:ATP6AP1|527:ATP6V0C|533:ATP6V0B|1513:CTSK|54:ACP5|4312:MMP1|4314:MMP3|1514:CTSL1|1437:CSF2|6352:CCL5|6347:CCL2|6348:CCL3|6349:CCL3L1|414062:CCL3L3|6364:CCL20|6374:CXCL5|6372:CXCL6|3576:IL8|6387:CXCL12|7423:VEGFB|5228:PGF|7422:VEGFA|2321:FLT1|284:ANGPT1|7010:TEK|3458:IFNG|2919:CXCL1	Osteopetrosis|Rheumatoid arthritis	Etanercept (genetical recombination) (JAN)|Adalimumab (genetical recombination) (JAN)|Infliximab (genetical recombination) (JAN)|Abatacept (genetical recombination) (JAN)|Certolizumab pegol (genetical recombination) (JAN)|Golimumab (genetical recombination) (JAN)	Rheumatoid arthritis (RA) is a chronic autoimmune joint disease where persistent inflammation affects bone remodeling leading to progressive bone destruction. In RA, abnormal activation of the immune system elevates pro-inflammatory cytokines and chemokines levels, which can promote synovial angiogenesis and leukocyte infiltration. The synovium forms a hyperplastic pannus with infiltrated macrophage-like and fibroblast-like synoviocytes and invades joints by secreting proteinases and inducing osteoclast differentiation.
hsa00790	Folate biosynthesis - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	2643:GCH1|251:ALPPL2|248:ALPI|250:ALPP|249:ALPL|1719:DHFR|2356:FPGS|8836:GGH|5805:PTS|6697:SPR|5860:QDPR|4337:MOCS1|4338:MOCS2|200895:DHFRL1	Phenylketonuria (PKU)|Hypophosphatasia|Primary torsion dystonia (PTD)|Dihydrofolate reductase (DHFR) deficiency	Methotrexate (JP16/USP/INN)|Methotrexate sodium|Pralatrexate (USAN/INN)|Trimetrexate (USAN/INN)|Trimetrexate glucuronate (USAN)	
hsa04727	GABAergic synapse - Homo sapiens (human)	Organismal Systems; Nervous System	81539:SLC38A1|54407:SLC38A2|2744:GLS|27165:GLS2|2571:GAD1|2572:GAD2|140679:SLC32A1|18:ABAT|2555:GABRA2|2554:GABRA1|2557:GABRA4|2556:GABRA3|2558:GABRA5|2559:GABRA6|2560:GABRB1|2562:GABRB3|2561:GABRB2|2566:GABRG2|2565:GABRG1|2567:GABRG3|2563:GABRD|2564:GABRE|55879:GABRQ|2568:GABRP|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|6714:SRC|5579:PRKCB|5578:PRKCA|5582:PRKCG|9001:HAP1|23710:GABARAPL1|11345:GABARAPL2|11337:GABARAP|4905:NSF|66008:TRAK2|5334:PLCL1|10243:GPHN|2569:GABRR1|200959:GABRR3|2570:GABRR2|773:CACNA1A|774:CACNA1B|775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|9568:GABBR2|2550:GABBR1|2773:GNAI3|2770:GNAI1|2771:GNAI2|2775:GNAO1|2782:GNB1|2783:GNB2|2784:GNB3|59345:GNB4|10681:GNB5|54331:GNG2|2785:GNG3|2786:GNG4|2787:GNG5|2788:GNG7|94235:GNG8|2790:GNG10|2791:GNG11|55970:GNG12|51764:GNG13|2792:GNGT1|2793:GNGT2|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|3763:KCNJ6|6529:SLC6A1|2752:GLUL|10991:SLC38A3|92745:SLC38A5|57468:SLC12A5|6538:SLC6A11|6540:SLC6A13	Hypokalemic periodic paralysis (HypoPP)|Episodic ataxias|Familial or sporadic hemiplegic migraine|Febrile seizures|Idiopathic generalied epilepsies (IGEs)|Congenital systemic glutamine deficiency (CSGD)|Cerebral palsy	Gamma-Aminobutyric acid (JAN)|Alprazolam (JP16/USP/INN)|Baclofen (JP16/USP/INN)|Chlordiazepoxide (JP16/USP/INN)|Clonazepam (JP16/USP/INN)|Diazepam (JP16/USP/INN)|Divalproex sodium (USP)|Estazolam (JP16/USAN/INN)|Flurazepam (JP16/INN)|Furosemide (JP16/USP/INN)|Lorazepam (JP16/USP/INN)|Temazepam (USP/INN)|Meprobamate (JAN/USP/INN)|Triazolam (JAN/USP/INN)|Valproic acid (USP)|Secobarbital (USP/INN)|Quazepam (JAN/USP/INN)|Prazepam (JP16/USAN/INN)|Pentobarbital (USP/INN)|Pentobarbital sodium (JAN/USP)|Phenobarbital (JP16/USP/INN)|Nitrazepam (JP16/USAN/INN)|Glutethimide (JAN/INN)|Vigabatrin (JAN/USAN/INN)|Topiramate (JAN/USAN/INN)|Propofol (JAN/USAN/INN)|Midazolam (JAN/USP/INN)|Amobarbital (JP16/INN)|Methaqualone (JAN/USAN/INN)|Chlordiazepoxide hydrochloride (JAN/USP)|Clorazepate dipotassium (JP16/USP)|Flurazepam hydrochloride (USP)|Midazolam hydrochloride (USAN)|Mephobarbital (JAN/USP)|Phenobarbital sodium (JAN/USP/INN)|Zolpidem tartrate (JP16/USAN)|Sodium valproate (JP16)|Thiamylal sodium (JP16)|Thiopental sodium (JP16/USP/INN)|Hexobarbital (JAN/INN)|Flunitrazepam (JP16/USAN/INN)|Bromazepam (JP16/USAN/INN)|Clobazam (JAN/USAN/INN)|Tofisopam (JP16/INN)|Cloxazolam (JP16/INN)|Oxazolam (JP16/INN)|Flutoprazepam (JP16/INN)|Flutazolam (JAN/INN)|Medazepam (JP16/INN)|Ethyl loflazepate (JAN/INN)|Secobarbital sodium (JAN/USP)|Mexazolam (JAN/INN)|Clotiazepam (JP16/INN)|Fludiazepam (JP16/INN)|Zopiclone (JAN/INN)|Flurazepam hydrochloride (JP16)|Etizolam (JP16/INN)|Rilmazafone hydrochloride hydrate (JAN)|Nimetazepam (JAN/INN)|Lormetazepam (JAN/USAN/INN)|Barbital (JP16/INN)|Brotizolam (JAN/USAN/INN)|Haloxazolam (JP16/INN)|Tiagabine hydrochloride (USP)|Amobarbital sodium (JP16/USP)|Pentobarbital calcium (JP16)|Pagoclone (USAN/INN)|Ocinaplon (USAN/INN)|Eszopiclone (JAN/USAN/INN)|Bretazenil (USAN/INN)|Clorazepate monopotassium (USAN)|Dextofisopam (USAN/INN)|Fospropofol disodium (USAN)|Gaboxadol (USAN/INN)|Ganaxolone (USAN/INN)|Levotofisopam (USAN/INN)|Medazepam hydrochloride (USAN)|Midazolam maleate (USAN)|Thiamylal|Ziconotide (USAN/INN)|Pentetrazol (INN)|Delorazepam (INN)|Sodium furosemide|Furosemide diolamine|Nordazepam (INN)|Phenobarbital diethylamine|Rilmazafone (INN)|Tiagabine (INN)|Calcium valproate|Ziconotide acetate|Zolpidem (INN)|Arbaclofen placarbil (USAN/INN)|Arbaclofen (USAN)	Gamma aminobutyric acid (GABA) is the most abundant inhibitory neurotransmitter in the mammalian central nervous system (CNS). When released in the synaptic cleft, GABA binds to three major classes of receptors: GABAA, GABAB, and GABAC receptors. GABAA and GABAC receptors are ionotropic and mediate fast GABA responses by triggering chloride channel openings, while GABAB receptors are metabotropic and mediate slower GABA responses by activating G-proteins and influencing second messenger systems. GABAA receptors, the major sites for fast inhibitory neurotransmission in the CNS, are regulated by phosphorylation mechanisms, affecting both their functional properties and their cell surface mobility and trafficking. GABA release by the presynaptic terminal is negatively regulated by GABAB autoreceptors, and is cleared from the extracellular space by GABA transporters (GATs) located either on the presynaptic terminal or neighboring glial cells.
hsa04621	NOD-like receptor signaling pathway - Homo sapiens (human)	Organismal Systems; Immune System	10392:NOD1|64127:NOD2|7205:TRIP6|8767:RIPK2|7189:TRAF6|8517:IKBKG|1147:CHUK|3551:IKBKB|4793:NFKBIB|4792:NFKBIA|4790:NFKB1|5970:RELA|3576:IL8|6347:CCL2|6352:CCL5|7124:TNF|3569:IL6|6885:MAP3K7|10454:TAB1|23118:TAB2|257397:TAB3|5594:MAPK1|5595:MAPK3|5602:MAPK10|5601:MAPK9|5599:MAPK8|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|64170:CARD9|841:CASP8|10910:SUGT1|55914:ERBB2IP|84674:CARD6|7128:TNFAIP3|22861:NLRP1|29108:PYCARD|834:CASP1|838:CASP5|114548:NLRP3|22900:CARD8|260434:PYDC1|4210:MEFV|9051:PSTPIP1|3320:HSP90AA1|3326:HSP90AB1|7184:HSP90B1|58484:NLRC4|59082:CARD18|4671:NAIP|3553:IL1B|3606:IL18|2919:CXCL1|2920:CXCL2|329:BIRC2|330:BIRC3|331:XIAP	Cryopyrin associated periodic syndrome (CAPS)|Blau syndrome|Crohn's disease|Pyogenic sterile arthritis, pyoderma gangrenosum, and acne (PAPA) syndrome|Familial Mediterranean fever (FMF)|Cocoon syndrome|Chronic Mucocutaneous Candidiasis (CMC)	Rilonacept (USAN/INN)|Canakinumab (genetical recombination) (JAN)	Specific families of pattern recognition receptors are responsible for detecting various pathogens and generating innate immune responses. The intracellular NOD-like receptor (NLR) family contains more than 20 members in mammals and plays a pivotal role in the recognition of intracellular ligands. NOD1 and NOD2, two prototypic NLRs, sense the cytosolic presence of the bacterial peptidoglycan fragments that escaped from endosomal compartments, driving the activation of NF-{kappa}B and MAPK, cytokine production and apoptosis. On the other hand, a different set of NLRs induces caspase-1 activation through the assembly of multiprotein complexes called inflammasomes. These NLRs include NALP1, NALP3 and Ipaf. The inflammasomes are critical for generating mature proinflammatory cytokines in concert with Toll-like receptor signaling pathway.
hsa05219	Bladder cancer - Homo sapiens (human)	Human Diseases; Cancers	2261:FGFR3|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|4609:MYC|11186:RASSF1|1613:DAPK3|23604:DAPK2|1612:DAPK1|1029:CDKN2A|4193:MDM2|7157:TP53|1026:CDKN1A|595:CCND1|1019:CDK4|5925:RB1|1871:E2F3|1869:E2F1|1870:E2F2|1950:EGF|2064:ERBB2|1956:EGFR|1890:TYMP|7423:VEGFB|5228:PGF|7422:VEGFA|7424:VEGFC|2277:FIGF|4312:MMP1|4313:MMP2|4318:MMP9|3576:IL8|999:CDH1|7057:THBS1|9252:RPS6KA5	Bladder cancer		The urothelium covers the luminal surface of almost the entire urinary tract, extending from the renal pelvis, through the ureter and bladder, to the proximal urethra. The majority of urothelial carcinoma are bladder carcinomas, and urothelial carcinomas of the renal pelvis and ureter account for only approximately 7% of the total. Urothelial tumours arise and evolve through divergent phenotypic pathways. Some tumours progress from urothelial hyperplasia to low-grade non-invasive superficial papillary tumours. More aggressive variants arise either from flat, high-grade carcinoma in situ (CIS) and progress to invasive tumours, or they arise de novo as invasive tumours. Low-grade papillary tumors frequently show a constitutive activation of the receptor tyrosine kinase-Ras pathway, exhibiting activating mutations in the HRAS and fibroblast growth factor receptor 3 (FGFR3) genes. In contrast, CIS and invasive tumors frequently show alterations in the TP53 and RB genes and pathways. Invasion and metastases are promoted by several factors that alter the tumour microenvironment, including the aberrant expression of  E-cadherins (E-cad), matrix metalloproteinases (MMPs), angiogenic factors such as vascular endothelial growth factor (VEGF).
hsa04060	Cytokine-cytokine receptor interaction - Homo sapiens (human)	Environmental Information Processing; Signaling Molecules and Interaction	2921:CXCL3|2920:CXCL2|2919:CXCL1|6374:CXCL5|6372:CXCL6|5473:PPBP|3576:IL8|4283:CXCL9|3627:CXCL10|6373:CXCL11|6387:CXCL12|10563:CXCL13|58191:CXCL16|5197:PF4V1|5196:PF4|9547:CXCL14|6846:XCL2|6375:XCL1|6376:CX3CL1|6360:CCL16|10344:CCL26|6346:CCL1|6361:CCL17|6362:CCL18|6369:CCL24|6358:CCL14|6367:CCL22|6364:CCL20|6370:CCL25|6363:CCL19|6366:CCL21|6347:CCL2|6348:CCL3|6349:CCL3L1|414062:CCL3L3|9560:CCL4L1|388372:CCL4L2|6351:CCL4|6355:CCL8|6354:CCL7|6357:CCL13|6356:CCL11|6352:CCL5|6359:CCL15|6368:CCL23|10850:CCL27|56477:CCL28|3569:IL6|3589:IL11|5008:OSM|3976:LIF|1270:CNTF|23529:CLCF1|1489:CTF1|1440:CSF3|3952:LEP|3565:IL4|3596:IL13|3592:IL12A|3593:IL12B|51561:IL23A|1437:CSF2|3562:IL3|3567:IL5|3558:IL2|3574:IL7|3578:IL9|3600:IL15|59067:IL21|85480:TSLP|2056:EPO|2689:GH2|2688:GH1|5617:PRL|7173:TPO|56034:PDGFC|5154:PDGFA|5155:PDGFB|7423:VEGFB|7422:VEGFA|7424:VEGFC|2277:FIGF|3082:HGF|1950:EGF|1435:CSF1|4254:KITLG|2323:FLT3LG|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3456:IFNB1|3467:IFNW1|56832:IFNK|338376:IFNE|3458:IFNG|3586:IL10|50604:IL20|11009:IL24|29949:IL19|50616:IL22|282618:IL29|282616:IL28A|282617:IL28B|55801:IL26|9966:TNFSF15|8743:TNFSF10|8600:TNFSF11|8742:TNFSF12|7124:TNF|4049:LTA|4050:LTB|8740:TNFSF14|356:FASLG|959:CD40LG|970:CD70|944:TNFSF8|8744:TNFSF9|7292:TNFSF4|8995:TNFSF18|8741:TNFSF13|10673:TNFSF13B|1896:EDA|7040:TGFB1|7042:TGFB2|7043:TGFB3|3625:INHBB|3626:INHBC|83729:INHBE|3624:INHBA|268:AMH|650:BMP2|655:BMP7|8200:GDF5|3605:IL17A|27190:IL17B|64806:IL25|3552:IL1A|3553:IL1B|3606:IL18|3579:CXCR2|3577:CXCR1|2833:CXCR3|7852:CXCR4|643:CXCR5|10663:CXCR6|57007:CXCR7|2829:XCR1|1524:CX3CR1|1237:CCR8|1235:CCR6|10803:CCR9|1233:CCR4|1236:CCR7|729230:CCR2|1234:CCR5|1230:CCR1|1232:CCR3|2826:CCR10|3570:IL6R|3572:IL6ST|3590:IL11RA|3977:LIFR|9180:OSMR|1271:CNTFR|1441:CSF3R|3953:LEPR|3566:IL4R|3597:IL13RA1|3594:IL12RB1|3595:IL12RB2|149233:IL23R|1438:CSF2RA|1439:CSF2RB|3563:IL3RA|3568:IL5RA|3559:IL2RA|3560:IL2RB|3561:IL2RG|3575:IL7R|3581:IL9R|3601:IL15RA|50615:IL21R|64109:CRLF2|2057:EPOR|2690:GHR|5618:PRLR|4352:MPL|5156:PDGFRA|5159:PDGFRB|2321:FLT1|3791:KDR|2324:FLT4|4233:MET|1956:EGFR|1436:CSF1R|3815:KIT|2322:FLT3|3454:IFNAR1|3455:IFNAR2|3459:IFNGR1|3460:IFNGR2|3587:IL10RA|3588:IL10RB|53832:IL20RA|53833:IL20RB|58985:IL22RA1|116379:IL22RA2|163702:IL28RA|8793:TNFRSF10D|8794:TNFRSF10C|8795:TNFRSF10B|8797:TNFRSF10A|4982:TNFRSF11B|8792:TNFRSF11A|8718:TNFRSF25|51330:TNFRSF12A|27242:TNFRSF21|4804:NGFR|7133:TNFRSF1B|7132:TNFRSF1A|4055:LTBR|8764:TNFRSF14|8771:TNFRSF6B|355:FAS|958:CD40|939:CD27|943:TNFRSF8|3604:TNFRSF9|7293:TNFRSF4|8784:TNFRSF18|608:TNFRSF17|23495:TNFRSF13B|115650:TNFRSF13C|10913:EDAR|60401:EDA2R|55504:TNFRSF19|84957:RELT|7048:TGFBR2|7046:TGFBR1|92:ACVR2A|93:ACVR2B|90:ACVR1|91:ACVR1B|269:AMHR2|659:BMPR2|657:BMPR1A|658:BMPR1B|23765:IL17RA|55540:IL17RB|3554:IL1R1|3556:IL1RAP|7850:IL1R2|8809:IL18R1|8807:IL18RAP|80301:PLEKHO2	Chemokine receptor defect|Congenital amegakaryocytic thrombocytopenia (CAMT)|Leprosy|Type I diabetes mellitus|46,XY disorders of sex development (Other)|Heterotaxy|Ectodermal dysplasia|Loeys-Dietz syndrome (LDS)|Familial thoracic aortic aneurysm and dissection (TAAD)|Macular degeneration|Tumor necrosis factor receptor-associated periodic syndrome (TRAPS)|Cold-induced sweating syndrome (CISS) and Crisponi syndrome (CRISPS)|Juvenile polyposis syndrome|Hereditary mixed polyposis syndrome|Chronic Mucocutaneous Candidiasis (CMC)|Pulmonary alveolar proteinosis (PAP)	Thiamazole (JP16/INN)|Propylthiouracil (JP16/USP/INN)|Etanercept (genetical recombination) (JAN)|Interferon alfa-2a (genetical recombination) (JAN)|Interferon beta-1b (genetical recombination) (JAN)|Interferon gamma-1b (USAN/INN)|Imatinib mesilate (JAN)|Gefitinib (JAN/USAN/INN)|Tocilizumab (genetical recombination) (JAN)|Adalimumab (genetical recombination) (JAN)|Infliximab (genetical recombination) (JAN)|Somatropin (genetical recombination) (JAN)|Celmoleukin (genetical recombination) (JP16)|Interferon alfacon-1 (genetical recombination) (JAN)|Interferon alfa-2b (genetical recombination) (JAN)|Peginterferon alfa-2a (genetical recombination) (JAN)|Peginterferon alfa-2b (generical recombination) (JAN)|Teceleukin (genetical recombination) (JP16)|Anakinra (USAN/INN)|Basiliximab (genetical recombination) (JAN)|Becaplermin (USAN/INN)|Ancriviroc (USAN/INN)|Axitinib (JAN/USAN)|Epoetin alfa (genetical recombination) (JAN)|Epoetin beta (genetical recombination) (JAN)|Filgrastim (genetical recombination) (JAN)|Nartograstim (genetical recombination) (JAN)|Lenograstim (genetical recombination) (JAN)|Interferon beta (JAN)|Interferon alfa (BALL-1) (JAN)|Canertinib dihydrochloride (USAN)|Interferon gamma-1a (genetical recombination) (JAN)|Certolizumab pegol (genetical recombination) (JAN)|Cetuximab (genetical recombination) (JAN)|Daclizumab (USAN/INN)|Daniplestim (USAN/INN)|Darbepoetin alfa (genetical recombination) (JAN)|Dasatinib (INN)|Denileukin diftitox (USAN/INN)|Denosumab (genetical recombination) (JAN)|Eltrombopag olamine (JAN/USAN)|Erlotinib hydrochloride (JAN/USAN)|Lapatinib tosilate hydrate (JAN)|Epoetin delta (USAN)|Golimumab (genetical recombination) (JAN)|Interferon alfa-n1 (USAN)|Interferon beta-1a (genetical recombination) (JAN)|Leridistim (USAN/INN)|Lestaurtinib (USAN/INN)|Mepolizumab (USAN/INN)|Metreleptin (USAN/INN)|Midostaurin (USAN/INN)|Panitumumab (genetical recombination) (JAN)|Pazopanib hydrochloride (JAN/USAN)|Pegaptanib sodium (JAN/USAN)|Pegnartograstim (USAN/INN)|Pegvisomant (genetical recombination) (JAN)|Pelitinib (USAN/INN)|Ranibizumab (genetical recombination) (JAN)|Semaxanib (USAN/INN)|Somatrem (genetical recombination) (JAN)|Tandutinib (USAN/INN)|Sorafenib tosilate (JAN)|Vatalanib (USAN/INN)|Vicriviroc maleate (USAN)|Sunitinib malate (JAN/USAN)|Vandetanib (JAN/USAN/INN)|Bevacizumab (genetical recombination) (JAN)|Nilotinib hydrochloride hydrate (JAN)|Dasatinib hydrate (JAN)|Aplaviroc hydrochloride (USAN)|Rilonacept (USAN/INN)|Maraviroc (JAN/INN)|Motesanib|Pegfilgrastim (INN)|Methylthiouracil (INN)|Benzylthiouracil|Erlotinib (INN)|Imatinib (INN)|Lapatinib (INN)|Sorafenib (USAN/INN)|Sunitinib (INN)|Interferon gamma-n1 (JAN)|Albinterferon alfa-2b (USAN)|Bevasiranib sodium (USAN)|Cediranib (USAN/INN)|Cediranib maleate (JAN/USAN)|Motesanib diphosphate (USAN)|Neratinib (INN/USAN)|Nilotinib (USAN/INN)|Plerixafor (USAN/INN)|Romiplostim (genetical recombination) (JAN)|Canakinumab (genetical recombination) (JAN)|Aflibercept (genetical recombination) (JAN)|Tivozanib (USAN/INN)|Afatinib (USAN/INN)|Afatinib maleate (JAN)|Amuvatinib (USAN/INN)|Amuvatinib hydrochloride (USAN)|Lenvatinib (USAN/INN)|Lenvatinib mesylate (USAN)|Quizartinib (USAN/INN)|Quizartinib dihydrochloride (USAN)|Zalutumumab (USAN/INN)|Cabozantinib (USAN)|Crenolanib (USAN)|Crenolanib besylate (USAN)|Regorafenib (USAN/INN)|Tivantinib (USAN/INN)	Cytokines are soluble extracellular proteins or glycoproteins that are crucial intercellular regulators and mobilizers of cells engaged in innate as well as adaptive inflammatory host defenses, cell growth, differentiation, cell death, angiogenesis, and development and repair processes aimed at the restoration of homeostasis. Cytokines are released by various cells in the body, usually in response to an activating stimulus, and they induce responses through binding to specific receptors on the cell surface of target cells. Cytokines can be grouped by structure into different families and their receptors can likewise be grouped.
hsa04721	Synaptic vesicle cycle - Homo sapiens (human)	Organismal Systems; Nervous System	140679:SLC32A1|6571:SLC18A2|6570:SLC18A1|6572:SLC18A3|57084:SLC17A6|57030:SLC17A7|246213:SLC17A8|6857:SYT1|6844:VAMP2|5864:RAB3A|22999:RIMS1|6804:STX1A|2054:STX2|112755:STX1B|6809:STX3|6812:STXBP1|23025:UNC13A|10497:UNC13B|440279:UNC13C|10814:CPLX2|10815:CPLX1|339302:CPLX4|594855:CPLX3|773:CACNA1A|774:CACNA1B|4905:NSF|8775:NAPA|26052:DNM3|1785:DNM2|10059:DNM1L|1759:DNM1|1211:CLTA|1212:CLTB|8218:CLTCL1|1213:CLTC|161:AP2A2|160:AP2A1|163:AP2B1|1173:AP2M1|1175:AP2S1|523:ATP6V1A|526:ATP6V1B2|525:ATP6V1B1|528:ATP6V1C1|245973:ATP6V1C2|51382:ATP6V1D|529:ATP6V1E1|90423:ATP6V1E2|9296:ATP6V1F|9550:ATP6V1G1|534:ATP6V1G2|127124:ATP6V1G3|8992:ATP6V0E1|155066:ATP6V0E2|535:ATP6V0A1|50617:ATP6V0A4|23545:ATP6V0A2|10312:TCIRG1|9114:ATP6V0D1|245972:ATP6V0D2|51606:ATP6V1H|527:ATP6V0C|533:ATP6V0B|6616:SNAP25	Early infantile epileptic encephalopathy|Centronuclear myopathy|Episodic ataxias|Familial or sporadic hemiplegic migraine	Reserpine (JP16/USP/INN)|Ziconotide (USAN/INN)|Tetrabenazine (JAN/INN)|Ziconotide acetate	Communication between neurons is mediated by the release of neurotransmitter from synaptic vesicles (SVs). At the nerve terminal, SVs cycle through repetitive episodes of exocytosis and endocytosis. SVs are filled with neurotransmitters by active transport. The loaded SVs are then docked at a specialized region of the presynaptic plasma membrane known as the active zone, where they undergo a priming reaction. Upon arrival of an action potential, Ca2+ enters through voltage-gated channels and neurotransmitter is released by exocytosis, usually in less than a millisecond. After fusion, the vesicle is retrieved by endocytosis and reloaded for another round of exocytosis.
hsa03430	Mismatch repair - Homo sapiens (human)	Genetic Information Processing; Replication and Repair	6742:SSBP1|5395:PMS2|4292:MLH1|2956:MSH6|4436:MSH2|4437:MSH3|27030:MLH3|5981:RFC1|5982:RFC2|5984:RFC4|5985:RFC5|5983:RFC3|5111:PCNA|9156:EXO1|6117:RPA1|6118:RPA2|6119:RPA3|29935:RPA4|5424:POLD1|5425:POLD2|10714:POLD3|57804:POLD4|3978:LIG1	Mismatch repair deficiency		DNA mismatch repair (MMR) is a highly conserved biological pathway that plays a key role in maintaining genomic stability. MMR corrects DNA mismatches generated during DNA replication, thereby preventing mutations from becoming permanent in dividing cells. MMR also suppresses homologous recombination and was recently shown to play a role in DNA damage signaling. Defects in MMR are associated with genome-wide instability, predisposition to certain types of cancer including HNPCC, resistance to certain chemotherapeutic agents, and abnormalities in meiosis and sterility in mammalian systems.|The Escherichia coli MMR pathway has been extensively studied and is well characterized. In E. coli, the mismatch-activated MutS-MutL-ATP complex licenses MutH to incise the nearest unmethylated GATC sequence. UvrD and an exonuclease generate a gap. This gap is filled by pol III and DNA ligase. The GATC sites are then methylated by Dam. Several human MMR proteins have been identified based on their homology to E. coli MMR proteins. These include human homologs of MutS and MutL. Although E. coli MutS and MutL proteins are homodimers, human MutS and MutL homologs are heterodimers. The role of hemimethylated dGATC sites as a signal for strand discrimination is not conserved from E. coli to human. Human MMR is presumed to be nick-directed in vivo, and is thought to discriminate daughter and template strands using a strand-specific nick.
hsa03450	Non-homologous end-joining - Homo sapiens (human)	Genetic Information Processing; Replication and Repair	2547:XRCC6|7520:XRCC5|64421:DCLRE1C|5591:PRKDC|27343:POLL|27434:POLM|1791:DNTT|3981:LIG4|7518:XRCC4|79840:NHEJ1|10111:RAD50|4361:MRE11A|2237:FEN1	Ataxia with ocular apraxia (AOA)|Severe combined immunodeficiency with microcephaly, growth retardation, and sensitivity to ionizing radiation		Nonhomologous end joining (NHEJ) eliminates DNA double-strand breaks (DSBs) by direct ligation. NHEJ involves binding of the KU heterodimer to double-stranded DNA ends, recruitment of DNA-PKcs (MRX complex in yeast), processing of ends, and recruitment of the DNA ligase IV (LIG4)-XRCC4 complex, which brings about ligation. A recent study shows that bacteria accomplish NHEJ using just two proteins (Ku and DNA ligase), whereas eukaryotes require many factors. NHEJ repairs DSBs at all stages of the cell cycle, bringing about the ligation of two DNA DSBs without the need for sequence homology, and so is error-prone.
hsa05340	Primary immunodeficiency - Homo sapiens (human)	Human Diseases; Immune Diseases	100:ADA|3575:IL7R|3561:IL2RG|64421:DCLRE1C|5896:RAG1|5897:RAG2|915:CD3D|916:CD3E|5788:PTPRC|920:CD4|925:CD8A|926:CD8B|326:AIRE|6890:TAP1|6891:TAP2|3932:LCK|7535:ZAP70|5993:RFX5|5994:RFXAP|8625:RFXANK|4261:CIITA|100132941:uncharacterized|100291917:uncharacterized|973:CD79A|29760:BLNK|695:BTK|8517:IKBKG|958:CD40|959:CD40LG|7374:UNG|57379:AICDA|29851:ICOS|115650:TNFRSF13C|930:CD19|23495:TNFRSF13B|3543:IGLL1|3718:JAK3	Agammaglobulinemias|Hyper IgM syndromes, autosomal recessive type|Common variable immunodeficiency (CVID)|T-B+Severe combined immunodeficiencies (SCIDs)|T-B-Severe combined immunodeficiencies (SCIDs)|Combined immunodeficiencies (CIDs)|Ectodermal dysplasia associated immunodeficiency (EDA-ID)|Other well-defined immunodeficiency syndromes|Bare lymphocyte syndrome (BLS) type1|Bare lymphocyte syndrome (BLS) type2		Primary immunodeficiencies (PIs) are a heterogeneous group of disorders, which affect cellular and humoral immunity or non-specific host defense mechanisms mediated by complement proteins, and cells such as phagocytes and natural killer (NK) cells. These disorders of the immune system cause increased susceptibility to infection, autoimmune disease, and malignancy. Most of PIs are due to genetic defects that affect cell maturation or function at different levels during hematopoiesis. Disruption of the cellular immunity is observed in patients with defects in T cells or both T and B cells. These cellular immunodeficiencies comprise 20% of all PIs. Disorders of humoral immunity affect B-cell differentiation and antibody production. They account for 70% of all PIs.
hsa04726	Serotonergic synapse - Homo sapiens (human)	Organismal Systems; Nervous System	7166:TPH1|121278:TPH2|1644:DDC|6571:SLC18A2|6570:SLC18A1|775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|3358:HTR2C|3357:HTR2B|3356:HTR2A|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|3708:ITPR1|3709:ITPR2|3710:ITPR3|5579:PRKCB|5578:PRKCA|5582:PRKCG|5594:MAPK1|5595:MAPK3|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|1562:CYP2C18|1559:CYP2C9|1557:CYP2C19|1558:CYP2C8|1565:CYP2D6|1573:CYP2J2|260293:CYP4X1|240:ALOX5|239:ALOX12|242:ALOX12B|246:ALOX15|247:ALOX15B|5742:PTGS1|5743:PTGS2|9177:HTR3B|3359:HTR3A|170572:HTR3C|200909:HTR3D|285242:HTR3E|3360:HTR4|3362:HTR6|3363:HTR7|2778:GNAS|111:ADCY5|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|3781:KCNN2|3751:KCND2|2560:GABRB1|2562:GABRB3|2561:GABRB2|10411:RAPGEF3|351:APP|3355:HTR1F|3354:HTR1E|3351:HTR1B|3352:HTR1D|3350:HTR1A|3361:HTR5A|2773:GNAI3|2770:GNAI1|2771:GNAI2|2775:GNAO1|2782:GNB1|2783:GNB2|2784:GNB3|59345:GNB4|10681:GNB5|54331:GNG2|2785:GNG3|2786:GNG4|2787:GNG5|2788:GNG7|94235:GNG8|2790:GNG10|2791:GNG11|55970:GNG12|51764:GNG13|2792:GNGT1|2793:GNGT2|836:CASP3|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|773:CACNA1A|774:CACNA1B|3760:KCNJ3|3763:KCNJ6|3765:KCNJ9|3762:KCNJ5|7220:TRPC1|6532:SLC6A4|4129:MAOB|4128:MAOA|1843:DUSP1	Neurodegeneration with brain iron accumulation (NBIA)|Aromatic L-amino acid decarboxylase (AADC) deficiency|Cerebral amyloid angiopathy (CAA)	Reserpine (JP16/USP/INN)|Chlorpromazine (USP/INN)|Cisapride (USAN/INN)|Clozapine (JAN/USP/INN)|Isoniazid (JP16/USP/INN)|Mazindol (JAN/USP/INN)|Levomepromazine (USAN/INN)|Zolmitriptan (JAN/USAN/INN)|Sumatriptan (JAN/USP/INN)|Phenelzine sulfate (USP)|Carbidopa hydrate (JP16)|Naratriptan hydrochloride (JAN/USAN)|Rizatriptan benzoate (JAN/USAN)|Sumatriptan succinate (JAN/USAN)|Methysergide maleate (USP)|Selegiline hydrochloride (JAN/USP)|Chlorpromazine hydrochloride (JP16/USP)|Nefazodone hydrochloride (USAN)|Tranylcypromine sulfate (USP XXI)|Lazabemide hydrochloride (JAN/USAN)|Milnacipran hydrochloride (JAN/USAN)|Ergometrine maleate (JP16)|Duloxetine hydrochloride (JAN/USAN)|Amezinium metilsulfate (JAN)|Sarpogrelate hydrochloride (JP16)|Safrazine hydrochloride (JAN)|Ziprasidone hydrochloride hydrate (JAN)|Eletriptan hydrobromide (JAN/USAN)|Ziprasidone mesylate (USAN)|Toloxatone (INN)|Brofaromine (INN)|Moclobemide (USAN/INN)|Rasagiline mesylate (USAN)|Befloxatone (INN)|Pargyline hydrochloride (USAN)|Sibutramine hydrochloride hydrate (JAN)|Agomelatine (INN)|Iproniazid (INN)|Isocarboxazid (INN)|Cimoxatone (INN)|Almotriptan (USAN)|Almotriptan malate (USAN)|Ladostigil tartrate (USAN)|Clorgiline (INN)|Chlorpromazine hibenzate (JAN)|Caroxazone (USAN/INN)|Dexfenfluramine hydrochloride (USAN)|Selegiline (USAN/INN)|Elzasonan citrate (USAN)|Elzasonan hydrochloride (USAN)|Chlorpromazine phenolphthalinate (JAN)|Fenfluramine hydrochloride (USAN)|Lazabemide (USAN/INN)|Lurasidone hydrochloride (JAN/USAN)|Metrenperone (USAN/INN)|Milacemide hydrochloride (USAN)|Lorcaserin hydrochloride (USAN)|Nialamide (INN)|Iproclozide (INN)|Dexfenfluramine (INN)|Iproniazid phosphate|Phenelzine (BAN)|Pargyline (INN)|Rasagiline (USAN/INN)|Sarpogrelate (INN)|Sibutramine (INN)|Tetrabenazine (JAN/INN)|Tranylcypromine (INN)	Serotonin (5-Hydroxytryptamine, 5-HT) is a monoamine neurotransmitter that plays important roles in physiological functions such as learning and memory, emotion, sleep, pain, motor function and endocrine secretion, as well as in pathological states including abnormal mood and cognition. Once released from presynaptic axonal terminals, 5-HT binds to receptors, which have been divided into 7 subfamilies on the basis of conserved structures and signaling mechanisms. These families include the ionotropic 5-HT3 receptors and G-protein-coupled 5-HT receptors, the 5-HT1 (Gi /Go -coupled), 5-HT2(Gq-coupled), 5-HT4/6/7 (Gs-coupled) and 5-HT5 receptors. Presynaptically localized 5-HT1B receptors are thought to be the autoreceptors that suppress excess 5-HT release. 5-HT's actions are terminated by transporter- mediated reuptake into neurons, leading to catabolism by monoamine oxidase.
hsa00040	Pentose and glucuronate interconversions - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	2990:GUSB|9365:KL|7363:UGT2B4|574537:UGT2A2|7367:UGT2B17|7365:UGT2B10|7364:UGT2B7|7366:UGT2B15|54577:UGT1A7|10720:UGT2B11|54490:UGT2B28|54579:UGT1A5|54659:UGT1A3|54657:UGT1A4|54578:UGT1A6|54576:UGT1A8|54600:UGT1A9|10941:UGT2A1|54575:UGT1A10|79799:UGT2A3|54658:UGT1A1|7358:UGDH|7360:UGP2|51084:CRYL1|729020:rcRPE|6120:RPE|9942:XYLB|231:AKR1B1|51181:DCXR|27294:DHDH|219:ALDH1B1|224:ALDH3A2|217:ALDH2|57016:AKR1B10	Pentosuria|Familial tumoral calcinosis (FTC)		
hsa00514	Other types of O-glycan biosynthesis - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	8473:OGT|29954:POMT2|10585:POMT1|146664:MGAT5B|55624:POMGNT1|2683:B4GALT1|8704:B4GALT2|8703:B4GALT3|7363:UGT2B4|574537:UGT2A2|7367:UGT2B17|7365:UGT2B10|7364:UGT2B7|7366:UGT2B15|54577:UGT1A7|10720:UGT2B11|54490:UGT2B28|54579:UGT1A5|54659:UGT1A3|54657:UGT1A4|54578:UGT1A6|54576:UGT1A8|54600:UGT1A9|10941:UGT2A1|54575:UGT1A10|79799:UGT2A3|54658:UGT1A1|10690:FUT9|2529:FUT7|2526:FUT4|6487:ST3GAL3|9486:CHST10|23275:POFUT2|23509:POFUT1|5986:RFNG|3955:LFNG|4242:MFNG|6480:ST6GAL1|84620:ST6GAL2|145173:B3GALTL|56983:POGLUT1|283464:GXYLT1|727936:GXYLT2|23127:GLT25D2|79709:GLT25D1|8985:PLOD3	Dystroglycanopathy|Congenital muscular dystrophies (CMD/MDC)|Limb-girdle muscular dystrophy (LGMD)|Nonsyndromic autosomal recessive mental retardation (NS-ARMR)|Peters anomaly|Lysyl hydroxylase 3 (LH3) deficiency		O-mannosyl glycans are a type of O-glycans that are found both in eukaryotes and prokaryotes. Biosynthesis of O-mannosyl glycans is initiated by the transfer of mannose from Man-P-Dol to serine or threonine residue, which is catalyzed by protein O-mannosyltransferases POMT1 and POMT2. Defects of these genes are linked to human diseases, such as muscular dystrophies caused by reduced O-mannosylation of alpha-dystroglycan in skeletal muscles [DS:H00120].
hsa04062	Chemokine signaling pathway - Homo sapiens (human)	Organismal Systems; Immune System	2921:CXCL3|2920:CXCL2|2919:CXCL1|6374:CXCL5|6372:CXCL6|5473:PPBP|3576:IL8|4283:CXCL9|3627:CXCL10|6373:CXCL11|6387:CXCL12|10563:CXCL13|58191:CXCL16|5197:PF4V1|5196:PF4|9547:CXCL14|6846:XCL2|6375:XCL1|6376:CX3CL1|6347:CCL2|6348:CCL3|6349:CCL3L1|414062:CCL3L3|9560:CCL4L1|388372:CCL4L2|6351:CCL4|6352:CCL5|6355:CCL8|6354:CCL7|6357:CCL13|6356:CCL11|6359:CCL15|6368:CCL23|6363:CCL19|6366:CCL21|6364:CCL20|6370:CCL25|10850:CCL27|56477:CCL28|6360:CCL16|10344:CCL26|6346:CCL1|6361:CCL17|6362:CCL18|6369:CCL24|6358:CCL14|6367:CCL22|3579:CXCR2|3577:CXCR1|2833:CXCR3|7852:CXCR4|643:CXCR5|10663:CXCR6|2829:XCR1|1524:CX3CR1|1237:CCR8|1235:CCR6|10803:CCR9|1233:CCR4|1236:CCR7|729230:CCR2|1234:CCR5|1230:CCR1|1232:CCR3|2826:CCR10|3717:JAK2|3718:JAK3|6772:STAT1|6773:STAT2|6774:STAT3|6777:STAT5B|2773:GNAI3|2770:GNAI1|2771:GNAI2|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|4067:LYN|3055:HCK|2268:FGR|6714:SRC|25759:SHC2|6464:SHC1|53358:SHC3|399694:SHC4|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|5894:RAF1|673:BRAF|5604:MAP2K1|5594:MAPK1|5595:MAPK3|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|207:AKT1|208:AKT2|10000:AKT3|2309:FOXO3|1147:CHUK|3551:IKBKB|8517:IKBKG|4792:NFKBIA|4793:NFKBIB|4790:NFKB1|5970:RELA|2931:GSK3A|2932:GSK3B|3702:ITK|10451:VAV3|7409:VAV1|7410:VAV2|5879:RAC1|5880:RAC2|5058:PAK1|998:CDC42|7454:WAS|8976:WASL|387:RHOA|6093:ROCK1|9475:ROCK2|2782:GNB1|2783:GNB2|2784:GNB3|59345:GNB4|10681:GNB5|54331:GNG2|2785:GNG3|2786:GNG4|2787:GNG5|2788:GNG7|94235:GNG8|2790:GNG10|2791:GNG11|55970:GNG12|51764:GNG13|2792:GNGT1|2793:GNGT2|57580:PREX1|9844:ELMO1|1794:DOCK2|5747:PTK2|5829:PXN|9564:BCAR1|1399:CRKL|1398:CRK|2185:PTK2B|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|10235:RASGRP2|5906:RAP1A|5908:RAP1B|56288:PARD3|26230:TIAM2|7074:TIAM1|653361:NCF1|6011:GRK1|131890:GRK7|156:ADRBK1|157:ADRBK2|2868:GRK4|2869:GRK5|2870:GRK6|409:ARRB2|408:ARRB1|5579:PRKCB|5580:PRKCD|5590:PRKCZ	PTEN hamartoma tumor syndrome (PHTS)|Osteoporosis, lymphedema, anhydrotic ectodermal dysplasia with immunodeficiency (OLEDAID)|Incontinentia pigmenti|Macular degeneration|Cocoon syndrome|Growth hormone insensitivity with immunodeficiency|Chronic Mucocutaneous Candidiasis (CMC)	Bosutinib (USAN)|Lestaurtinib (USAN/INN)|Vicriviroc maleate (USAN)|Aplaviroc hydrochloride (USAN)|Maraviroc (JAN/INN)|Sorafenib (USAN/INN)|Plerixafor (USAN/INN)|Bosutinib hydrate (JAN)|Tofacitinib citrate (JAN/USAN)|Ruxolitinib (USAN/INN)|Ruxolitinib phosphate (JAN/USAN)|Tofacitinib (USAN)	Inflammatory immune response requires the recruitment of leukocytes to the site of inflammation upon foreign insult. Chemokines are small chemoattractant peptides that provide directional cues for the cell trafficking and thus are vital for protective host response. In addition, chemokines regulate plethora of biological processes of hematopoietic cells to lead cellular activation, differentiation and survival.|The chemokine signal is transduced by chemokine receptors (G-protein coupled receptors) expressed on the immune cells. After receptor activation, the alpha- and beta-gamma-subunits of G protein dissociate to activate diverse downstream pathways resulting in cellular polarization and actin reorganization. Various members of small GTPases are involved in this process. Induction of nitric oxide and production of reactive oxygen species are as well regulated by chemokine signal via calcium mobilization and diacylglycerol production.
hsa05145	Toxoplasmosis - Homo sapiens (human)	Human Diseases; Infectious Diseases	3458:IFNG|3459:IFNGR1|3460:IFNGR2|3716:JAK1|3717:JAK2|6772:STAT1|4261:CIITA|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|345611:IRGM|4843:NOS2|8651:SOCS1|4615:MYD88|3654:IRAK1|51135:IRAK4|7189:TRAF6|6885:MAP3K7|10454:TAB1|23118:TAB2|5594:MAPK1|5595:MAPK3|5602:MAPK10|5601:MAPK9|5599:MAPK8|5606:MAP2K3|5608:MAP2K6|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|1147:CHUK|3551:IKBKB|8517:IKBKG|4792:NFKBIA|4793:NFKBIB|4790:NFKB1|5970:RELA|3592:IL12A|3593:IL12B|7124:TNF|596:BCL2|598:BCL2L1|330:BIRC3|331:XIAP|329:BIRC2|23643:LY96|7099:TLR4|3306:HSPA2|3310:HSPA6|3304:HSPA1B|3305:HSPA1L|3312:HSPA8|3303:HSPA1A|7097:TLR2|284217:LAMA1|3908:LAMA2|3911:LAMA5|3909:LAMA3|3910:LAMA4|3912:LAMB1|3913:LAMB2|3914:LAMB3|22798:LAMB4|3915:LAMC1|3918:LAMC2|10319:LAMC3|3655:ITGA6|3688:ITGB1|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|3949:LDLR|7132:TNFRSF1A|841:CASP8|836:CASP3|54205:CYCS|842:CASP9|2773:GNAI3|2770:GNAI1|2771:GNAI2|2775:GNAO1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5163:PDK1|207:AKT1|208:AKT2|10000:AKT3|572:BAD|959:CD40LG|958:CD40|10105:PPIF|1234:CCR5|240:ALOX5|3586:IL10|3587:IL10RA|3588:IL10RB|7297:TYK2|6774:STAT3|7040:TGFB1|7042:TGFB2|7043:TGFB3|112401:BIRC8|79444:BIRC7	Toxoplasmosis		Toxoplasma gondii is an obligate intracellular parasite that is prevalent worldwide. The tachyzoite form acquired by oral ingestion downmodulates proinflammatory signaling pathways via various mechanisms. During early infection, nuclear translocation of NFkB is temporally blocked and p38 MAPK phosphorylation is prevented, suppressing IL-12 production. Another pathway for IL-12 induction occurs through CCR5 dependent pathway, but parasitic induction of an eicosanoid LXA4 contributes to the downregulation of IL-12. Direct activation of STAT3 by the parasite enhance anti-inflammatory function of IL-10 and TGF beta. T. gondii can cause lifelong chronic infection by establishing an anti-apoptotic environment through induction of bcl-2 or IAPs and by redirecting LDL-mediated cholesterol transport to scavenge nutrients from the host.
hsa00072	Synthesis and degradation of ketone bodies - Homo sapiens (human)	Metabolism; Lipid Metabolism	3158:HMGCS2|3157:HMGCS1|3155:HMGCL|5019:OXCT1|64064:OXCT2|38:ACAT1|39:ACAT2|622:BDH1|56898:BDH2	Alpha-methylacetoacetic aciduria|Succinyl CoA:3-oxoacid CoA transferase (SCOT) deficiency|HMG-CoA synthase (HMGCS) deficiency		
hsa03420	Nucleotide excision repair - Homo sapiens (human)	Genetic Information Processing; Replication and Repair	9978:RBX1|8450:CUL4B|8451:CUL4A|1642:DDB1|1643:DDB2|7508:XPC|5887:RAD23B|5886:RAD23A|1069:CETN2|1161:ERCC8|2074:ERCC6|1022:CDK7|4331:MNAT1|902:CCNH|2071:ERCC3|2068:ERCC2|404672:GTF2H5|2965:GTF2H1|2966:GTF2H2|728340:GTF2H2C|730394:GTF2H2D|2967:GTF2H3|2968:GTF2H4|2073:ERCC5|7507:XPA|6117:RPA1|6118:RPA2|6119:RPA3|29935:RPA4|2072:ERCC4|2067:ERCC1|5424:POLD1|5425:POLD2|10714:POLD3|57804:POLD4|5426:POLE|5427:POLE2|54107:POLE3|56655:POLE4|5111:PCNA|5981:RFC1|5982:RFC2|5984:RFC4|5985:RFC5|5983:RFC3|3978:LIG1	Disorders of nucleotide excision repair|Syndromic X-linked mental retardation|Macular degeneration		Nucleotide excision repair (NER) is a mechanism to recognize and repair bulky DNA damage caused by compounds, environmental carcinogens, and exposure to UV-light. In humans hereditary defects in the NER pathway are linked to at least three diseases: xeroderma pigmentosum (XP), Cockayne syndrome (CS), and trichothiodystrophy (TTD). The repair of damaged DNA involves at least 30 polypeptides within two different sub-pathways of NER known as transcription-coupled repair (TCR-NER) and global genome repair (GGR-NER). TCR refers to the expedited repair of lesions located in the actively transcribed strand of genes by RNA polymerase II (RNAP II). In GGR-NER the first step of damage recognition involves XPC-hHR23B complex together with XPE complex (in prokaryotes, uvrAB complex). The following steps of GGR-NER and TCR-NER are similar.
hsa05034	Alcoholism - Homo sapiens (human)	Human Diseases; Substance Dependence	10013:HDAC6|10014:HDAC5|10488:CREB3|10645:CAMKK2|10681:GNB5|111:ADCY5|116443:GRIN3A|116444:GRIN3B|121504:HIST4H4|126961:HIST2H3C|128312:HIST3H2BB|135:ADORA2A|136:ADORA2B|1385:CREB1|1386:ATF2|1388:ATF6B|1392:CRH|148327:CREB3L4|158983:H2BFWT|163688:CALML6|1644:DDC|1812:DRD1|1813:DRD2|2030:SLC29A1|221613:HIST1H2AA|2354:FOSB|255626:HIST1H2BA|25759:SHC2|2770:GNAI1|2771:GNAI2|2773:GNAI3|2775:GNAO1|2778:GNAS|2782:GNB1|2783:GNB2|2784:GNB3|2785:GNG3|2786:GNG4|2787:GNG5|2788:GNG7|2790:GNG10|2791:GNG11|2792:GNGT1|2793:GNGT2|286436:H2BFM|2885:GRB2|2902:GRIN1|2903:GRIN2A|2904:GRIN2B|2905:GRIN2C|2906:GRIN2D|3012:HIST1H2AE|3013:HIST1H2AD|3014:H2AFX|3015:H2AFZ|3017:HIST1H2BD|3018:HIST1H2BB|3020:H3F3A|3021:H3F3B|3065:HDAC1|3066:HDAC2|317772:HIST2H2AB|3265:HRAS|333932:HIST2H3A|369:ARAF|3845:KRAS|399694:SHC4|4128:MAOA|4129:MAOB|440093:H3F3C|440689:HIST2H2BF|468:ATF4|474381:H2AFB2|474382:H2AFB1|4852:NPY|4893:NRAS|4915:NTRK2|51564:HDAC7|5173:PDYN|51764:GNG13|51806:CALML5|53358:SHC3|54331:GNG2|5499:PPP1CA|5500:PPP1CB|5501:PPP1CC|554313:HIST2H4B|55506:H2AFY2|5566:PRKACA|5569:PKIA|55766:H2AFJ|55869:HDAC8|5594:MAPK1|5595:MAPK3|55970:GNG12|5604:MAP2K1|5894:RAF1|59345:GNB4|627:BDNF|6464:SHC1|64764:CREB3L2|6531:SLC6A3|653604:HIST2H3D|6570:SLC18A1|6571:SLC18A2|6654:SOS1|6655:SOS2|673:BRAF|7054:TH|723790:HIST2H2AA4|79885:HDAC11|801:CALM1|805:CALM2|808:CALM3|810:CALML3|814:CAMK4|8290:HIST3H3|8294:HIST1H4I|8329:HIST1H2AI|8330:HIST1H2AK|8331:HIST1H2AJ|8332:HIST1H2AL|8334:HIST1H2AC|8335:HIST1H2AB|8336:HIST1H2AM|8337:HIST2H2AA3|8338:HIST2H2AC|8339:HIST1H2BG|8340:HIST1H2BL|8341:HIST1H2BN|8342:HIST1H2BM|8343:HIST1H2BF|8344:HIST1H2BE|8345:HIST1H2BH|8346:HIST1H2BI|8347:HIST1H2BC|8348:HIST1H2BO|8349:HIST2H2BE|8350:HIST1H3A|8351:HIST1H3D|8352:HIST1H3C|8353:HIST1H3E|8354:HIST1H3I|8355:HIST1H3G|8356:HIST1H3J|8357:HIST1H3H|8358:HIST1H3B|8359:HIST1H4A|8360:HIST1H4D|8361:HIST1H4F|8362:HIST1H4K|8363:HIST1H4J|8364:HIST1H4C|8365:HIST1H4H|8366:HIST1H4B|8367:HIST1H4E|8368:HIST1H4L|8369:HIST1H4G|8370:HIST2H4A|83740:H2AFB3|83933:HDAC10|84152:PPP1R1B|84254:CAMKK1|84699:CREB3L3|8520:HAT1|85235:HIST1H2AH|85236:HIST1H2BK|8841:HDAC3|8968:HIST1H3F|8969:HIST1H2AG|8970:HIST1H2BJ|90993:CREB3L1|92815:HIST3H2A|94235:GNG8|94239:H2AFV|9555:H2AFY|9586:CREB5|9734:HDAC9|9759:HDAC4			Alcoholism, also called dependence on alcohol (ethanol), is a chronic relapsing disorder that is progressive and has serious detrimental health outcomes. As one of the primary mediators of the rewarding effects of alcohol, dopaminergic ventral tegmental area (VTA) projections to the nucleus accumbens (NAc) have been identified. Acute exposure to alcohol stimulates dopamine release into the NAc, which activates D1 receptors, stimulating PKA signaling and subsequent CREB-mediated gene expression,  whereas chronic alcohol exposure leads to an adaptive downregulation of this pathway, in particular of CREB function. The decreased CREB function in the NAc may promote the intake of drugs of abuse to achieve an increase in reward and thus may be involved in the regulation of positive affective states of addiction. PKA signaling also affects NMDA receptor activity and may  play an important role in neuroadaptation in response to chronic alcohol exposure.
hsa04966	Collecting duct acid secretion - Homo sapiens (human)	Organismal Systems; Excretory System	523:ATP6V1A|526:ATP6V1B2|525:ATP6V1B1|9550:ATP6V1G1|534:ATP6V1G2|127124:ATP6V1G3|528:ATP6V1C1|245973:ATP6V1C2|51382:ATP6V1D|529:ATP6V1E1|90423:ATP6V1E2|9296:ATP6V1F|8992:ATP6V0E1|155066:ATP6V0E2|535:ATP6V0A1|50617:ATP6V0A4|23545:ATP6V0A2|10312:TCIRG1|527:ATP6V0C|9114:ATP6V0D1|245972:ATP6V0D2|495:ATP4A|496:ATP4B|6521:SLC4A1|10723:SLC12A7|1188:CLCNKB|760:CA2	Combined proximal and distal renal tubular acidosis (RTA type 3)|Distal renal tubular acidosis (RTA type 1)	Lansoprazole (JAN/USP/INN)|Omeprazole (JP16/USP/INN)|Sodium rabeprazole (JP16)|Omeprazole sodium (USAN)|Tenatoprazole (JAN/INN)|Esomeprazole magnesium hydrate (JAN)|Pantoprazole Sodium Hydrate (JAN)|Esomeprazole sodium (USAN)|Omeprazole magnesium (USAN)|Omeprazole sodium injection (JAN)|Pantoprazole (USAN/INN)|Timoprazole (INN)|Picoprazole (INN)|Leminoprazole (INN)|Esomeprazole (INN)|Rabeprazole (INN)|Dexlansoprazole (INN/USAN)|Esomeprazole potassium (USAN)	One of the important roles of the collecting duct segment of the kidney nephron is acid secretion. As daily food intake loads acid into the body, urinary acid excretion is essential, and urine pH can drop as low as 4.5. The alpha-intercalated cell of collecting duct is the main responsible for hydrogen secretion into the urine. The carbon dioxide, which is generated in the cells and enters from the blood, is changed to carbonic acid. This carbonic acid is divided into hydrogen ion and bicarbonate ion. Intracellular CA II catalyses the formation of these ions. The hydrogen ion is secreted into the lumen by the luminal H(+)-ATPase. The bicarbonate ion is transported to the blood side by the anion exchanger type 1. Hydrogen ion in the lumen is trapped by urinary buffers. These include ammonium and phosphate.
hsa04120	Ubiquitin mediated proteolysis - Homo sapiens (human)	Genetic Information Processing; Folding, Sorting and Degradation	7317:UBA1|10055:SAE1|10054:UBA2|9039:UBA3|7318:UBA7|55236:UBA6|7319:UBE2A|7320:UBE2B|11065:UBE2C|7325:UBE2E2|7324:UBE2E1|7323:UBE2D3|7322:UBE2D2|7321:UBE2D1|10477:UBE2E3|51619:UBE2D4|140739:UBE2F|7326:UBE2G1|7327:UBE2G2|7328:UBE2H|7329:UBE2I|51465:UBE2J1|118424:UBE2J2|7332:UBE2L3|9246:UBE2L6|9040:UBE2M|7334:UBE2N|389898:UBE2NL|63893:UBE2O|55585:UBE2Q1|92912:UBE2Q2|134111:UBE2QL1|997:CDC34|54926:UBE2R2|27338:UBE2S|148581:UBE2U|55284:UBE2W|65264:UBE2Z|3093:UBE2K|57448:BIRC6|7337:UBE3A|89910:UBE3B|9690:UBE3C|57154:SMURF1|64750:SMURF2|83737:ITCH|11059:WWP1|11060:WWP2|9320:TRIP12|4734:NEDD4|23327:NEDD4L|10075:HUWE1|51366:UBR5|8925:HERC1|8924:HERC2|8916:HERC3|26091:HERC4|9354:UBE4A|10277:UBE4B|10273:STUB1|23759:PPIL2|27339:PRPF19|22888:UBOX5|4193:MDM2|23624:CBLC|868:CBLB|867:CBL|5071:PARK2|6477:SIAH1|5371:PML|7189:TRAF6|4214:MAP3K1|64326:RFWD2|25898:RCHY1|330:BIRC3|331:XIAP|329:BIRC2|8554:PIAS1|51588:PIAS4|10401:PIAS3|9063:PIAS2|84447:SYVN1|378884:NHLRC1|326:AIRE|23295:MGRN1|672:BRCA1|55120:FANCL|4281:MID1|22954:TRIM32|4591:TRIM37|9978:RBX1|8454:CUL1|6500:SKP1|23291:FBXW11|8945:BTRC|6502:SKP2|55294:FBXW7|26232:FBXO2|26272:FBXO4|8453:CUL2|6921:TCEB1|6923:TCEB2|7428:VHL|8452:CUL3|9817:KEAP1|55958:KLHL9|90293:KLHL13|9886:RHOBTB1|23221:RHOBTB2|8450:CUL4B|8451:CUL4A|1642:DDB1|1643:DDB2|1161:ERCC8|55070:DET1|9616:RNF7|8065:CUL5|8651:SOCS1|9021:SOCS3|9820:CUL7|26259:FBXW8|51529:ANAPC11|29882:ANAPC2|991:CDC20|51343:FZR1|64682:ANAPC1|996:CDC27|29945:ANAPC4|51433:ANAPC5|8881:CDC16|51434:ANAPC7|8697:CDC23|10393:ANAPC10|246184:CDC26|25847:ANAPC13|112401:BIRC8|79444:BIRC7	Prader-Willi and Angelman syndromes|3M syndrome|von Hippel-Lindau syndrome|Opitz-GBBB syndrome|Syndromic X-linked mental retardation|Progressive myoclonic epilepsy (PME)		Protein ubiquitination plays an important role in eukaryotic cellular processes. It mainly functions as a signal for 26S proteasome dependent protein degradation. The addition of ubiquitin to proteins being degraded is performed by a reaction cascade consisting of three enzymes, named E1 (ubiquitin activating enzyme), E2 (ubiquitin conjugating enzyme), and E3 (ubiquitin ligase). Each E3 has specificity to its substrate, or proteins to be targeted by ubiquitination. Many E3s are discovered in eukaryotes and they are classified into four types: HECT type, U-box type, single RING-finger type, and multi-subunit RING-finger type. Multi-subunit RING-finger E3s are exemplified by cullin-Rbx E3s and APC/C. They consist of a RING-finger-containing subunit (RBX1 or RBX2) that functions to bind E2s, a scaffold-like cullin molecule, adaptor proteins, and a target recognizing subunit that binds substrates.
hsa00071	Fatty acid metabolism - Homo sapiens (human)	Metabolism; Lipid Metabolism	38:ACAT1|39:ACAT2|30:ACAA1|10449:ACAA2|3032:HADHB|3033:HADH|3030:HADHA|1962:EHHADH|1892:ECHS1|8310:ACOX3|51:ACOX1|35:ACADS|34:ACADM|33:ACADL|36:ACADSB|37:ACADVL|2639:GCDH|2180:ACSL1|2182:ACSL4|2181:ACSL3|51703:ACSL5|23305:ACSL6|23205:ACSBG1|81616:ACSBG2|1375:CPT1B|1374:CPT1A|126129:CPT1C|1376:CPT2|1632:ECI1|10455:ECI2|1579:CYP4A11|284541:CYP4A22|126:ADH1C|131:ADH7|124:ADH1A|125:ADH1B|127:ADH4|128:ADH5|130:ADH6|219:ALDH1B1|224:ALDH3A2|217:ALDH2|501:ALDH7A1|223:ALDH9A1	Sjogren-Larsson syndrome|Glutaric acidemia|Peroxisomal beta-oxidation enzyme deficiency|Disorders of fatty-acid oxidation	Cyanamide (JP16)|Disulfiram (JP16/USP/INN)|Fomepizole (USAN/INN)|Oxfenicine (USAN/INN)	
hsa05162	Measles - Homo sapiens (human)	Human Diseases; Infectious Diseases	4478:MSN|10332:CLEC4M|30835:CD209|6869:TACR1|4179:CD46|6504:SLAMF1|4068:SH2D1A|2534:FYN|1796:DOK1|3596:IL13|3565:IL4|915:CD3D|916:CD3E|917:CD3G|940:CD28|3558:IL2|3559:IL2RA|3560:IL2RB|3561:IL2RG|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|207:AKT1|208:AKT2|10000:AKT3|2932:GSK3B|3716:JAK1|3718:JAK3|6774:STAT3|6776:STAT5A|6777:STAT5B|23586:DDX58|64135:IFIH1|57506:MAVS|9641:IKBKE|29110:TBK1|3661:IRF3|51284:TLR7|54106:TLR9|4615:MYD88|3654:IRAK1|51135:IRAK4|3665:IRF7|1147:CHUK|7097:TLR2|7099:TLR4|7189:TRAF6|6885:MAP3K7|23118:TAB2|4793:NFKBIB|4792:NFKBIA|4790:NFKB1|5970:RELA|1459:CSNK2A2|1457:CSNK2A1|1460:CSNK2B|7128:TNFAIP3|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3456:IFNB1|3552:IL1A|3553:IL1B|3569:IL6|3592:IL12A|3593:IL12B|100132941:uncharacterized|100291917:uncharacterized|2213:FCGR2B|3454:IFNAR1|3455:IFNAR2|10399:GNB2L1|7297:TYK2|6772:STAT1|6773:STAT2|10379:IRF9|3458:IFNG|3459:IFNGR1|3460:IFNGR2|3717:JAK2|4938:OAS1|4940:OAS3|4939:OAS2|103:ADAR|4599:MX1|595:CCND1|894:CCND2|896:CCND3|9134:CCNE2|898:CCNE1|1019:CDK4|1021:CDK6|1017:CDK2|1027:CDKN1B|9367:RAB9A|51209:RAB9B|3306:HSPA2|3310:HSPA6|3304:HSPA1B|3305:HSPA1L|3312:HSPA8|3303:HSPA1A|8667:EIF3H|5610:EIF2AK2|27102:EIF2AK1|440275:EIF2AK4|9451:EIF2AK3|1965:EIF2S1|25898:RCHY1|7157:TP53|7161:TP73|27113:BBC3|356:FASLG|355:FAS|8743:TNFSF10|8793:TNFRSF10D|8794:TNFRSF10C|8795:TNFRSF10B|8797:TNFRSF10A|5588:PRKCQ|868:CBLB	Measles		Measles virus (MV) is highly contagious virus that leads infant death worldwide. Humans are the unique natural reservoir for this virus. It causes severe immunosuppression favouring secondary bacterial infections. Several MV proteins have been suggested to disturb host immunity. After infection of host lymphoid cells via SLAM, MV inhibits cytokine response by direct interference with host signaling systems. Three proteins (P, V, and C) associate with Jak/STAT proteins in interferon-triggered pathway and other important proteins related to apoptosis. Interaction between MV and host brings about the shift towards a Th2 response by decreasing IL-12 production and induces lymphopenia by suppressing cell proliferation.
hsa05010	Alzheimer's disease - Homo sapiens (human)	Human Diseases; Neurodegenerative Diseases	102:ADAM10|6868:ADAM17|351:APP|8883:NAE1|322:APBB1|2597:GAPDH|23621:BACE1|25825:BACE2|55851:PSENEN|5663:PSEN1|5664:PSEN2|23385:NCSTN|51107:APH1A|3416:IDE|4311:MME|4723:NDUFV1|4729:NDUFV2|4731:NDUFV3|4694:NDUFA1|4695:NDUFA2|4696:NDUFA3|4697:NDUFA4|56901:NDUFA4L2|4698:NDUFA5|4700:NDUFA6|4701:NDUFA7|4702:NDUFA8|4704:NDUFA9|4705:NDUFA10|4706:NDUFAB1|126328:NDUFA11|55967:NDUFA12|51079:NDUFA13|4707:NDUFB1|4708:NDUFB2|4709:NDUFB3|4710:NDUFB4|4711:NDUFB5|4712:NDUFB6|4713:NDUFB7|4714:NDUFB8|4715:NDUFB9|4716:NDUFB10|54539:NDUFB11|4719:NDUFS1|4720:NDUFS2|4722:NDUFS3|4724:NDUFS4|4725:NDUFS5|4726:NDUFS6|374291:NDUFS7|4728:NDUFS8|4717:NDUFC1|4718:NDUFC2|6389:SDHA|6390:SDHB|6391:SDHC|6392:SDHD|7386:UQCRFS1|4519:CYTB|1537:CYC1|7384:UQCRC1|7385:UQCRC2|7388:UQCRH|440567:UQCRHL|7381:UQCRB|27089:UQCRQ|29796:UQCR10|10975:UQCR11|4514:COX3|4512:COX1|4513:COX2|1327:COX4I1|84701:COX4I2|9377:COX5A|1329:COX5B|1337:COX6A1|1339:COX6A2|1340:COX6B1|125965:COX6B2|1345:COX6C|1347:COX7A2|1346:COX7A1|9167:COX7A2L|1349:COX7B|170712:COX7B2|1350:COX7C|1351:COX8A|341947:COX8C|498:ATP5A1|506:ATP5B|509:ATP5C1|513:ATP5D|514:ATP5E|4508:ATP6|515:ATP5F1|518:ATP5G3|516:ATP5G1|517:ATP5G2|10476:ATP5H|539:ATP5O|522:ATP5J|4509:ATP8|3028:HSD17B10|4023:LPL|348:APOE|4035:LRP1|355:FAS|7132:TNFRSF1A|8772:FADD|841:CASP8|637:BID|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|572:BAD|54205:CYCS|317:APAF1|842:CASP9|836:CASP3|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|2902:GRIN1|2903:GRIN2A|2904:GRIN2B|2905:GRIN2C|2906:GRIN2D|775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|5594:MAPK1|5595:MAPK3|6263:RYR3|3708:ITPR1|3709:ITPR2|3710:ITPR3|488:ATP2A2|489:ATP2A3|487:ATP2A1|22926:ATF6|2081:ERN1|4842:NOS1|823:CAPN1|824:CAPN2|8851:CDK5R1|1020:CDK5|4137:MAPT|2932:GSK3B|840:CASP7|6622:SNCA|7124:TNF|3553:IL1B|9451:EIF2AK3|100532726:NDUFC2-KCTD14	Alzheimer's disease (AD)|Mitochondrial respiratory chain deficiencies (MRCD)	Memantine hydrochloride (JAN/USAN)|Memantine (INN)|Begacestat (USAN/INN)|Tarenflurbil (INN/USAN)|Semagacestat (USAN/INN)|Avagacestat (USAN)	Alzheimer's disease (AD) is a chronic disorder that slowly destroys neurons and causes serious cognitive disability. AD is associated with senile plaques and neurofibrillary tangles (NFTs). Amyloid-beta (Abeta), a major component of senile plaques, has various pathological effects on cell and organelle function. The extracellular Abeta oligomers may activate caspases through activation of cell surface death receptors. Alternatively, intracellular Abeta may contribute to pathology by facilitating tau hyper-phosphorylation, disrupting mitochondria function, and triggering calcium dysfunction. To date genetic studies have revealed four genes that may be linked to autosomal dominant or familial early onset AD (FAD). These four genes include: amyloid precursor protein (APP), presenilin 1 (PS1), presenilin 2 (PS2) and apolipoprotein E (ApoE). All mutations associated with APP and PS proteins can lead to an increase in the production of Abeta peptides, specfically the more amyloidogenic form, Abeta42. FAD-linked PS1 mutation downregulates the unfolded protein response and leads to vulnerability to ER stress.
hsa04530	Tight junction - Homo sapiens (human)	Cellular Processes; Cell Communication	9080:CLDN9|7122:CLDN5|9071:CLDN10|9075:CLDN2|1365:CLDN3|9074:CLDN6|9073:CLDN8|5010:CLDN11|23562:CLDN14|9076:CLDN1|24146:CLDN15|26285:CLDN17|53842:CLDN22|10686:CLDN16|49861:CLDN20|149461:CLDN19|137075:CLDN23|1366:CLDN7|1364:CLDN4|51208:CLDN18|100506658:OCLN|50848:F11R|58494:JAM2|83700:JAM3|150084:IGSF5|92359:CRB3|64398:MPP5|10207:INADL|50855:PARD6A|84552:PARD6G|84612:PARD6B|5584:PRKCI|5590:PRKCZ|56288:PARD3|3993:LLGL2|3996:LLGL1|998:CDC42|5516:PPP2CB|5515:PPP2CA|5518:PPP2R1A|5519:PPP2R1B|55844:PPP2R2D|5520:PPP2R2A|5522:PPP2R2C|5521:PPP2R2B|5579:PRKCB|5578:PRKCA|5582:PRKCG|5588:PRKCQ|5581:PRKCE|5580:PRKCD|5583:PRKCH|1459:CSNK2A2|1457:CSNK2A1|1460:CSNK2B|2773:GNAI3|2770:GNAI1|2771:GNAI2|8777:MPDZ|9218:VAPA|27134:TJP3|7082:TJP1|9414:TJP2|51776:ZAK|1499:CTNNB1|8531:CSDA|8189:SYMPK|55870:ASH1L|1019:CDK4|57530:CGN|60:ACTB|71:ACTG1|4633:MYL2|4636:MYL5|58498:MYL7|10398:MYL9|93408:MYL10|10627:MYL12A|103910:MYL12B|29895:MYLPF|22989:MYH15|4622:MYH4|8735:MYH13|4629:MYH11|4620:MYH2|4621:MYH3|4619:MYH1|4626:MYH8|4625:MYH7|4628:MYH10|57644:MYH7B|4627:MYH9|79784:MYH14|4624:MYH6|387:RHOA|4301:MLLT4|3265:HRAS|3845:KRAS|4893:NRAS|6237:RRAS|22800:RRAS2|22808:MRAS|8573:CASK|154810:AMOTL1|93643:TJAP1|3059:HCLS1|2017:CTTN|1496:CTNNA2|1495:CTNNA1|29119:CTNNA3|2035:EPB41|2036:EPB41L1|2037:EPB41L2|23136:EPB41L3|81:ACTN4|88:ACTN2|87:ACTN1|89:ACTN3|6714:SRC|7525:YES1|5865:RAB3B|5872:RAB13|11336:EXOC3|60412:EXOC4|9223:MAGI1|9863:MAGI2|260425:MAGI3|5728:PTEN|207:AKT1|208:AKT2|10000:AKT3|6709:SPTAN1	MYH9-related kidney diseases|Distal muscular dystrophies|Early infantile epileptic encephalopathy|Nephrotic syndrome and focal segmental glomerulosclerosis|Scapuloperoneal myopathy (SPM)|Myosin storage myopathy (MSM)|Neonatal ichthyosis-sclerosing cholangitis (NISCH) syndrome|Familial thoracic aortic aneurysm and dissection (TAAD)|Distal arthrogryposis (DA)|Band-like calcification with simplified gyration and polymicrogyria (BLC-PMG)|Trismus-pseudocamptodactyly syndrome|FG syndrome (FGS)|Pilomatricoma|VACTERL/VATER association|Hypomagnesemia		Epithelial tight junctions (TJs) are composed of at least three types of transmembrane protein -occludin, claudin and junctional adhesion molecules (JAMs)- and a cytoplasmic 'plaque' consisting of many different proteins that form large complexes. The transmembrane proteins mediate cell adhesion and are thought to constitute the intramembrane and paracellular diffusion barriers. The cytoplasmic 'plaque' contains three major multi-protein complexes consisting largely of scaffolding proteins, the ZO protein complex, the CRB3-Pals1-PATJ complex and the PAR-3-aPKC-PAR-6 complex. The ZO protein complex appears to organize the transmembrane proteins and couple them to other cytoplasmic proteins and to actin microfilaments. Two evolutionarily conserved protein complexes, the CRB3 and PAR complexes are involved in the establishment and maintenance of epithelial cell polarity. Besides these three protein complexes which seem to be constitutively associated at TJs, a number of proteins with different functions has been identified at TJs. These include additional scaffolding proteins like MUPP1 and MAGI-1, adaptor proteins, transcription regulators and RNA processing factors, regulatory proteins like small GTPases and G-proteins, kinases and phosphatases, and heat shock proteins. These are proposed to be involved in junction assembly, barrier regulation, gene transcription, and perhaps other, presently undefined pathways.
hsa05214	Glioma - Homo sapiens (human)	Human Diseases; Cancers	1950:EGF|7039:TGFA|1956:EGFR|5154:PDGFA|5155:PDGFB|5156:PDGFRA|5159:PDGFRB|3479:IGF1|3480:IGF1R|5335:PLCG1|5336:PLCG2|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|5579:PRKCB|5578:PRKCA|5582:PRKCG|25759:SHC2|6464:SHC1|53358:SHC3|399694:SHC4|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|2475:MTOR|5728:PTEN|1029:CDKN2A|4193:MDM2|7157:TP53|1026:CDKN1A|595:CCND1|1019:CDK4|1021:CDK6|5925:RB1|1871:E2F3|1869:E2F1|1870:E2F2	Glioma		Gliomas are the most common of the primary brain tumors and account for more than 40% of all central nervous system neoplasms. Gliomas include tumours that are composed predominantly of astrocytes (astrocytomas), oligodendrocytes (oligodendrogliomas), mixtures of various glial cells (for example,oligoastrocytomas) and ependymal cells (ependymomas). The most malignant form of infiltrating astrocytoma - glioblastoma multiforme (GBM) - is one of the most aggressive human cancers. GBM may develop de novo (primary glioblastoma) or by progression from low-grade or anaplastic astrocytoma (secondary glioblastoma).  Primary glioblastomas develop in older patients and typically show genetic alterations (EGFR amplification, p16/INK4a deletion, and PTEN mutations) at frequencies of 24-34%. Secondary glioblastomas develop in younger patients and frequently show overexpression of PDGF and CDK4 as well as p53 mutations (65%) and loss of Rb playing major roles in such transformations. Loss of PTEN has been implicated in both pathways, although it is much more common in the pathogenesis of primary GBM.
hsa04940	Type I diabetes mellitus - Homo sapiens (human)	Human Diseases; Endocrine and Metabolic Diseases	3630:INS|2571:GAD1|2572:GAD2|5798:PTPRN|5799:PTPRN2|1363:CPE|3329:HSPD1|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|941:CD80|942:CD86|940:CD28|3592:IL12A|3593:IL12B|3558:IL2|3458:IFNG|3133:HLA-E|3134:HLA-F|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|356:FASLG|355:FAS|5551:PRF1|3002:GZMB|4049:LTA|7124:TNF|3552:IL1A|3553:IL1B|3382:ICA1	Type I diabetes mellitus		Type I diabetes mellitus is a disease that results from autoimmune destruction of the insulin-producing beta-cells. Certain beta-cell proteins act as autoantigens after being processed by antigen-presenting cell (APC), such as macrophages and dendritic cells, and presented in a complex with MHC-II molecules on the surface of the APC. Then immunogenic signals from APC activate CD4+ T cells, predominantly of the Th1 subset. Antigen-activated Th1 cells produce IL-2 and IFNgamma. They activate macrophages and cytotoxic CD8+ T cells, and these effector cells may kill islet beta-cells by one or both of two types of mechanisms: (1) direct interactions of antigen-specific cytotoxic T cells with a beta-cell autoantigen-MHC-I complex on the beta-cell, and (2) non-specific inflammatory mediators, such as free radicals/oxidants and cytokines (IL-1, TNFalpha, TNFbeta, IFNgamma).|Type I diabetes is a polygenic disease. One of the principle determining genetic factors in diabetes incidence is the inheritance of mutant MHC-II alleles. Another plausible candidate gene is the insulin gene.
hsa04914	Progesterone-mediated oocyte maturation - Homo sapiens (human)	Organismal Systems; Endocrine System	5241:PGR|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|5602:MAPK10|5601:MAPK9|5599:MAPK8|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|2773:GNAI3|2770:GNAI1|2771:GNAI2|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|64506:CPEB1|387778:SPDYC|245711:SPDYA|1017:CDK2|983:CDK1|890:CCNA2|8900:CCNA1|4342:MOS|3320:HSP90AA1|3326:HSP90AB1|5604:MAP2K1|5594:MAPK1|5595:MAPK3|6195:RPS6KA1|6196:RPS6KA2|6197:RPS6KA3|27330:RPS6KA6|9088:PKMYT1|9133:CCNB2|891:CCNB1|85417:CCNB3|5347:PLK1|993:CDC25A|994:CDC25B|995:CDC25C|3630:INS|3479:IGF1|3480:IGF1R|207:AKT1|208:AKT2|10000:AKT3|5140:PDE3B|5139:PDE3A|3845:KRAS|369:ARAF|673:BRAF|5894:RAF1|699:BUB1|8379:MAD1L1|4085:MAD2L1|10459:MAD2L2|51343:FZR1|64682:ANAPC1|29882:ANAPC2|996:CDC27|29945:ANAPC4|51433:ANAPC5|8881:CDC16|51434:ANAPC7|8697:CDC23|10393:ANAPC10|51529:ANAPC11|246184:CDC26|25847:ANAPC13		Progesterone (JP16/USP/INN)|Norethisterone (JP16)|Amrinone (JAN/INN)|Danazol (JP16/USP/INN)|Dipyridamole (JP16/USP/INN)|Milrinone (JAN/USP/INN)|Mifepristone (USAN/INN)|Hydroxyprogesterone caproate (JAN/USP/INN)|Levonorgestrel (JAN/USP/INN)|Medroxyprogesterone acetate (JAN/USP)|Megestrol acetate (USAN)|Norethisterone acetate (JAN)|Norgestrel (JP16/USP/INN)|Pimobendan (JAN/USAN/INN)|Gestonorone caproate (JAN/USAN)|Dydrogesterone (JP16/USP/INN)|Ethynodiol diacetate (JAN/USP)|Chlormadinone acetate (JP16/USAN)|Allylestrenol (JAN/INN)|Lynestrenol (JAN/USAN)|Vesnarinone (JAN/USAN/INN)|Proxyphylline (JAN/INN)|Cilostazol (JP16/USAN/INN)|Olprinone hydrochloride hydrate (JAN)|Inamrinone lactate|Milrinone lactate|Desogestrel (USAN/INN)|Asoprisnil (USAN/INN)|Mecasermin (genetical recombination) (JAN)|Dienogest (JAN/USAN/INN)|Enoximone (USAN/INN)|Etonogestrel (USAN/INN)|Gestodene (USAN/INN)|Imazodan hydrochloride (USAN)|Indolidan (USAN/INN)|Isomazole hydrochloride (USAN)|Levosimendan (USAN/INN)|Lixazinone sulfate (USAN)|Mecasermin rinfabate (USAN/INN)|Medrogestone (USAN/INN)|Methynodiol diacetate (USAN)|Norgestimate (USP/INN)|Aminophylline hydrate (JP16)|Quingestanol acetate (USAN)|Norgestrienone (INN)|Nomegestrol (USAN/INN)|Demegestone (INN)|Chlormadinone (INN)|Etynodiol (INN)|Hydroxyprogesterone (INN)|Hydroxyprogesterone 17alfa-acetate|Medroxyprogesterone (INN)|Megestrol (INN)|Nomegestrol acetate (USAN)|Norethisterone enantate|Promegestone (INN)	Xenopus oocytes are naturally arrested at G2 of meiosis I. Exposure to either insulin/IGF-1 or the steroid hormone progesterone breaks this arrest and induces resumption of the two meiotic division cycles and maturation of the oocyte into a mature, fertilizable egg. This process is termed oocyte maturation. The transition is accompanied by an increase in maturation promoting factor (MPF or Cdc2/cyclin B) which precedes germinal vesicle breakdown (GVBD). Most reports point towards the Mos-MEK1-ERK2 pathway [where ERK is an extracellular signal-related protein kinase, MEK is a MAPK/ERK kinase and Mos is a p42(MAPK) activator] and the polo-like kinase/CDC25 pathway as responsible for the activation of MPF in meiosis, most likely triggered by a decrease in cAMP.
hsa04672	Intestinal immune network for IgA production - Homo sapiens (human)	Organismal Systems; Immune System	941:CD80|942:CD86|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|940:CD28|3558:IL2|3565:IL4|3567:IL5|3569:IL6|3586:IL10|7040:TGFB1|8741:TNFSF13|10673:TNFSF13B|23495:TNFRSF13B|608:TNFRSF17|115650:TNFRSF13C|100132941:uncharacterized|100291917:uncharacterized|57379:AICDA|958:CD40|959:CD40LG|29851:ICOS|23308:ICOSLG|10803:CCR9|3676:ITGA4|3695:ITGB7|6387:CXCL12|7852:CXCR4|10850:CCL27|56477:CCL28|2826:CCR10|6370:CCL25|8174:MADCAM1|4055:LTBR|9020:MAP3K14|3600:IL15|3601:IL15RA|5284:PIGR		Abatacept (genetical recombination) (JAN)|Valategrast hydrochloride (USAN)	The intestine is the largest lymphoid tissue in the body. One striking feature of intestinal immunity is its ability to generate great amounts of noninflammatory immunoglobulin A (IgA) antibodies that serve as the first line of defense against microorganisms. The basic map of IgA production includes induction of mucosal B cells in the Peyer's patches, circulation through the bloodstream and homing to intestinal mucosa of IgA-commited plasma cells, and local antibody production for export across the intestinal membranes. Multiple cytokines, including TGF-{beta}, IL-10, IL-4, IL-5, and IL-6, are required to promote IgA class switching and terminal differentiation process of the B cells. Secreted IgA promotes immune exclusion by entrapping dietary antigens and microorganisms in the mucus and functions for neutralization of toxins and pathogenic microbes.
hsa04130	SNARE interactions in vesicular transport - Homo sapiens (human)	Genetic Information Processing; Folding, Sorting and Degradation	6804:STX1A|2054:STX2|112755:STX1B|6809:STX3|6810:STX4|8676:STX11|415117:STX19|8417:STX7|8675:STX16|6811:STX5|55014:STX17|53407:STX18|143187:VTI1A|10490:VTI1B|9527:GOSR1|9570:GOSR2|662:BNIP1|8677:STX10|10228:STX6|9482:STX8|51272:BET1L|10282:BET1|55850:USE1|6616:SNAP25|8773:SNAP23|9342:SNAP29|116841:SNAP47|6843:VAMP1|6844:VAMP2|9341:VAMP3|8673:VAMP8|8674:VAMP4|10791:VAMP5|6845:VAMP7|10652:YKT6|9554:SEC22B	Pseudohypoparathyroidism|Cerebral dysgenesis, neuropathy, ichthyosis, and palmoplantar keratoderma syndrome		
hsa05222	Small cell lung cancer - Homo sapiens (human)	Human Diseases; Cancers	2272:FHIT|5915:RARB|6256:RXRA|6257:RXRB|6258:RXRG|7157:TP53|596:BCL2|54205:CYCS|317:APAF1|842:CASP9|4609:MYC|4149:MAX|8554:PIAS1|51588:PIAS4|10401:PIAS3|9063:PIAS2|1030:CDKN2B|1019:CDK4|1021:CDK6|595:CCND1|1163:CKS1B|6502:SKP2|1017:CDK2|9134:CCNE2|898:CCNE1|5925:RB1|1871:E2F3|1869:E2F1|1870:E2F2|1284:COL4A2|1286:COL4A4|1288:COL4A6|1287:COL4A5|1282:COL4A1|284217:LAMA1|3908:LAMA2|3911:LAMA5|3909:LAMA3|3910:LAMA4|3912:LAMB1|3913:LAMB2|3914:LAMB3|22798:LAMB4|3915:LAMC1|3918:LAMC2|10319:LAMC3|2335:FN1|3673:ITGA2|3674:ITGA2B|3675:ITGA3|3655:ITGA6|3685:ITGAV|3688:ITGB1|5747:PTK2|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5728:PTEN|207:AKT1|208:AKT2|10000:AKT3|1147:CHUK|3551:IKBKB|8517:IKBKG|4792:NFKBIA|4790:NFKB1|5970:RELA|330:BIRC3|331:XIAP|329:BIRC2|598:BCL2L1|7185:TRAF1|7186:TRAF2|7187:TRAF3|9618:TRAF4|7188:TRAF5|7189:TRAF6|5743:PTGS2|4843:NOS2|1027:CDKN1B|112401:BIRC8|79444:BIRC7	Small cell lung cancer		Lung cancer is a leading cause of cancer death among men and women in industrialized countries. Small cell lung carcinoma (SCLC) is a highly aggressive neoplasm, which accounts for approximately 25% of all lung cancer cases.  Molecular mechanisms altered in SCLC include induced expression of oncogene, MYC, and loss of tumorsuppressor genes, such as p53, PTEN, RB, and FHIT. The overexpression of MYC proteins in SCLC is largely a result of gene amplification. Such overexpression leads to more rapid proliferation and loss of terminal differentiation. Mutation or deletion of p53 or PTEN can lead to more rapid proliferation and reduced apoptosis. The retinoblastoma gene RB1 encodes a nuclear phosphoprotein that helps to regulate cell-cycle progression. The fragile histidine triad gene FHIT encodes the enzyme diadenosine triphosphate hydrolase, which is thought to have an indirect role in proapoptosis and cell-cycle control.
hsa04710	Circadian rhythm - mammal - Homo sapiens (human)	Organismal Systems; Environmental Adaptation	1453:CSNK1D|1454:CSNK1E|8863:PER3|8864:PER2|5187:PER1|1407:CRY1|1408:CRY2|406:ARNTL|9575:CLOCK|4862:NPAS2|9572:NR1D1|6095:RORA|6096:RORB|6097:RORC|8553:BHLHE40|79365:BHLHE41|9978:RBX1|8454:CUL1|6500:SKP1|23291:FBXW11|8945:BTRC|26224:FBXL3	Familial advanced sleep phase syndrome		
hsa04725	Cholinergic synapse - Homo sapiens (human)	Organismal Systems; Nervous System	1103:CHAT|43:ACHE|6572:SLC18A3|1128:CHRM1|1131:CHRM3|1133:CHRM5|2776:GNAQ|2767:GNA11|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|3708:ITPR1|3709:ITPR2|3710:ITPR3|5579:PRKCB|5578:PRKCA|5582:PRKCG|3784:KCNQ1|3785:KCNQ2|3786:KCNQ3|9132:KCNQ4|56479:KCNQ5|3759:KCNJ2|3768:KCNJ12|3761:KCNJ4|3770:KCNJ14|1129:CHRM2|1132:CHRM4|2773:GNAI3|2770:GNAI1|2771:GNAI2|2775:GNAO1|2782:GNB1|2783:GNB2|2784:GNB3|59345:GNB4|10681:GNB5|54331:GNG2|2785:GNG3|2786:GNG4|2787:GNG5|2788:GNG7|94235:GNG8|2790:GNG10|2791:GNG11|55970:GNG12|51764:GNG13|2792:GNGT1|2793:GNGT2|3760:KCNJ3|3763:KCNJ6|3265:HRAS|3845:KRAS|4893:NRAS|5604:MAP2K1|5594:MAPK1|5595:MAPK3|2353:FOS|1139:CHRNA7|1137:CHRNA4|1141:CHRNB2|1136:CHRNA3|1143:CHRNB4|8973:CHRNA6|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|1385:CREB1|468:ATF4|10488:CREB3|64764:CREB3L2|84699:CREB3L3|148327:CREB3L4|90993:CREB3L1|9586:CREB5|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|814:CAMK4|3717:JAK2|2534:FYN|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|596:BCL2|773:CACNA1A|774:CACNA1B|775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|60482:SLC5A7	Early infantile epileptic encephalopathy|Hypokalemic periodic paralysis (HypoPP)|Andersen-Tawil syndrome (ATS)|Episodic ataxias|Congenital myasthenic syndrome|Familial or sporadic hemiplegic migraine|Benign familial neonatal and infantile epilepsies|Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE)	Isoflurophate (USP)|Atropine (USP)|Scopolamine (INN)|Hyoscyamine (USP)|Physostigmine (USP)|Methyloctatropine bromide (JAN)|Chlorpromazine (USP/INN)|Tropicamide (JP16/USP/INN)|Oxybutynin (USAN/INN)|Propantheline bromide (JP16/USP/INN)|Carbachol (JAN/USP/INN)|Pilocarpine (JAN/USP)|Glycopyrronium bromide (JAN/INN)|Mecamylamine hydrochloride (USP)|Tolterodine (USAN/INN)|Cevimeline hydrochloride hydrate (JAN)|Donepezil hydrochloride (JP16/USAN)|Hyoscine methobromide (INN)|Dicyclomine hydrochloride (JAN/USP)|Hyoscyamine sulfate (USP)|Mepenzolate bromide (JP16/INN)|Methanthelinium bromide (INN)|Oxybutynin hydrochloride (JAN)|Tridihexethyl chloride (BAN)|Orphenadrine citrate (USP)|Benztropine mesilate (JAN)|Biperiden (JAN/USP/INN)|Procyclidine hydrochloride (USP)|Trihexyphenidyl hydrochloride (JP16/USP)|Chlorpromazine hydrochloride (JP16/USP)|Acetylcholine chloride (JP16/USP/INN)|Bethanechol chloride (JP16/USP)|Cyclopentolate hydrochloride (JP16/USP)|Hexocyclium metilsulfate (INN)|Homatropine hydrobromide (JP16/USP)|Isopropamide iodide (JAN/USP/INN)|Oxyphencyclimine hydrochloride (JAN)|Propiverine hydrochloride (JP16)|Atropine methonitrate (JAN/INN)|Trospium chloride (JAN/USAN/INN)|Profenamine hydrochloride (JAN)|Tolterodine tartrate (JAN/USAN)|Piperidolate hydrochloride (JAN)|Carpronium chloride (JAN/INN)|Tiemonium iodide (JAN/INN)|Distigmine bromide (JP16/INN)|Piroheptine hydrochloride (JAN)|Solifenacin succinate (JAN/USAN/INN)|Pirenzepine hydrochloride (USAN)|Methylbenactyzium bromide (JP16/INN)|Etomidoline (JAN/INN)|Prifinium bromide (JAN/INN)|Scopolamine butylbromide (JP16)|Diponium bromide (JAN/INN)|Butropium bromide (JP16/INN)|Trimebutine maleate (JP16)|Pipethanate hydrochloride (JAN)|Valethamate bromide (JAN)|Diphenylpiperidinomethyldioxolan iodide (JAN)|Hyoscyamine methylbromide (JAN)|Darifenacin hydrobromide (JAN/USAN)|Oxapium iodide (JP16/INN)|Metixene hydrochloride (JAN)|Tiquizium bromide (JAN/INN)|Tiotropium bromide hydrate (JAN)|Oxitropium bromide (JAN/INN)|Aclatonium napadisilate (JAN)|N-Methylscopolamine methylsulfate (JAN)|Pipethanate ethobromide (JAN)|Tacrine hydrochloride (USP)|Atropine sulfate (JP16/USP)|Homatropine methylbromide (USP)|Scopolamine hydrobromide hydrate (JP16)|Pilocarpine hydrochloride (JP16/USP)|Hexamethonium bromide (JAN/INN)|Ipratropium bromide hydrate (JP16)|Biperiden hydrochloride (JP16/USP)|Biperiden lactate (JAN/USP)|Flutropium bromide (JAN)|Timepidium bromide hydrate (JP16)|Rivastigmine tartrate|Dimetacrine (INN)|Orphenadrine hydrochloride|Aceclidine (USAN/INN)|Altinicline maleate (USAN)|Alvameline maleate (USAN)|Atropine oxide hydrochloride (USAN)|Benzetimide hydrochloride (USAN)|Ladostigil tartrate (USAN)|Mazaticol hydrochloride hydrate (JAN)|Chlorpromazine hibenzate (JAN)|Profenamine hibenzate (JAN)|Darifenacin (USAN/INN)|Dexetimide (USAN/INN)|Atropine methylbromide (JAN)|Rivastigmine (JAN/USAN/INN)|Chlorpromazine phenolphthalinate (JAN)|Esoxybutynin chloride (USAN)|Ethybenztropine (USAN)|Eucatropine hydrochloride (USP XXXII)|Galantamine (USAN/INN)|Hyoscyamine hydrobromide (USP)|Methacholine chloride (USAN/INN)|Milameline hydrochloride (USAN)|Pirenzepine hydrochloride hydrate (JP16)|Pilocarpine nitrate (USP)|Talsaclidine fumarate (USAN)|Imidafenacin (JAN/INN)|Velnacrine maleate (USAN)|Xanomeline (USAN)|Xanomeline tartrate (USAN)|Ziconotide (USAN/INN)|Cimetropium bromide (INN)|Choline alfoscerate (INN)|Atropine oxide (INN)|Benzatropine (INN)|Cevimeline (INN)|Cyclopentolate (INN)|Dicycloverine (INN)|Fentonium bromide (INN)|Mazaticol (INN)|Orphenadrine (INN)|Oxyphencyclimine (INN)|Pilocarpine borate|Piperidolate (INN)|Pipethanate (INN)|Pirenzepine (INN)|Piroheptine (INN)|Procyclidine (INN)|Profenamine (INN)|Propiverine (INN)|Solifenacin (INN)|Tacrine (INN)|Tiemonium methylsulfate|Trihexyphenidyl (INN)|Trimebutine (INN)|Ziconotide acetate|Ispronicline (INN/USAN)|Carpronium chloride hydrate (JAN)|Dexmecamylamine (USAN)|Dexmecamylamine hydrochloride (USAN)	Acetylcholine (ACh) is a neurotransmitter widely distributed in the central (and also peripheral, autonomic and enteric) nervous system (CNS). In the CNS, ACh facilitates many functions, such as learning, memory, attention and motor control. When released in the synaptic cleft, ACh binds to two distinct types of receptors: Ionotropic nicotinic acetylcholine receptors (nAChR) and metabotropic muscarinic acetylcholine receptors (mAChRs). The activation of nAChR by ACh leads to the rapid influx of Na+ and Ca2+ and subsequent cellular depolarization. Activation of mAChRs is relatively slow (milliseconds to seconds) and, depending on the subtypes present (M1-M5), they directly alter cellular homeostasis of phospholipase C, inositol trisphosphate, cAMP, and free calcium. In the cleft, ACh may also be hydrolyzed by acetylcholinesterase (AChE) into choline and acetate. The choline derived from ACh hydrolysis is recovered by a presynaptic high-affinity choline transporter (CHT).
hsa04970	Salivary secretion - Homo sapiens (human)	Organismal Systems; Digestive System	153:ADRB1|154:ADRB2|155:ADRB3|2778:GNAS|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|6844:VAMP2|148:ADRA1A|147:ADRA1B|146:ADRA1D|1131:CHRM3|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|5579:PRKCB|5578:PRKCA|5582:PRKCG|3708:ITPR1|3709:ITPR2|3710:ITPR3|6263:RYR3|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|4842:NOS1|2982:GUCY1A3|2977:GUCY1A2|2983:GUCY1B3|5593:PRKG2|5592:PRKG1|683:BST1|952:CD38|54831:BEST2|362:AQP5|476:ATP1A1|480:ATP1A4|478:ATP1A3|477:ATP1A2|481:ATP1B1|482:ATP1B2|483:ATP1B3|23439:ATP1B4|486:FXYD2|491:ATP2B2|490:ATP2B1|493:ATP2B4|492:ATP2B3|6558:SLC12A2|3783:KCNN4|3778:KCNMA1|6522:SLC4A2|6548:SLC9A1|55503:TRPV6|727897:MUC5B|4589:MUC7|5554:PRH1|5555:PRH2|653247:PRB2|5542:PRB1|1755:DMBT1|1469:CST1|1470:CST2|1471:CST3|1472:CST4|1473:CST5|3346:HTN1|6779:STATH|4069:LYZ|4025:LPO|820:CAMP|276:AMY1A|277:AMY1B|278:AMY1C	Familial amyloidosis	Noradrenaline (JP16)|Adrenaline (JP16)|Atropine (USP)|Ephedrine (USP)|Scopolamine (INN)|Hyoscyamine (USP)|Methyloctatropine bromide (JAN)|Atenolol (JP16/USP/INN)|Carvedilol (JAN/USAN/INN)|Clozapine (JAN/USP/INN)|Timolol (USAN)|Tropicamide (JP16/USP/INN)|Risperidone (JP16/USAN/INN)|Nadolol (JP16/USP/INN)|Olanzapine (JAN/USAN/INN)|Quetiapine fumarate (JAN/USAN)|Oxybutynin (USAN/INN)|Propantheline bromide (JP16/USP/INN)|Propranolol hydrochloride (JP16/USP)|Pseudoephedrine hydrochloride (USP)|Phenoxybenzamine hydrochloride (USP)|Phentolamine mesilate (JAN/INN)|Phenylephrine hydrochloride (JP16/USP)|Pindolol (JP16/USP/INN)|Carbachol (JAN/USP/INN)|Pilocarpine (JAN/USP)|Glycopyrronium bromide (JAN/INN)|Pimozide (JP16/USP/INN)|Sertindole (USAN/INN)|Acebutolol hydrochloride (JP16/USP)|Betaxolol hydrochloride (JP16/USP)|Carteolol hydrochloride (JP16/USP)|Labetalol hydrochloride (JP16/USP)|Metoprolol tartrate (JP16/USP)|Penbutolol sulfate (JP16/USP)|Timolol maleate (JP16/USP)|Guanadrel sulfate (USP)|Doxazosin mesilate (JP16)|Prazosin hydrochloride (JP16/USP)|Terazosin hydrochloride hydrate (JAN)|Dobutamine hydrochloride (JP16/USP)|Bisoprolol fumarate (JP16/USP)|Metoprolol succinate (USP)|Esmolol hydrochloride (JAN/USAN)|Tolterodine (USAN/INN)|Cevimeline hydrochloride hydrate (JAN)|Ergotamine tartrate (JP16/USP)|Methylergometrine maleate (JP16)|Salbutamol sulfate (JP16)|Bitolterol mesilate (JAN)|Orciprenaline sulfate (JP16)|Pirbuterol acetate (USAN)|Salmeterol xinafoate (JAN/USAN)|Terbutaline sulfate (JP16/USP)|Hyoscine methobromide (INN)|Hyoscyamine sulfate (USP)|Mepenzolate bromide (JP16/INN)|Methanthelinium bromide (INN)|Oxybutynin hydrochloride (JAN)|Tridihexethyl chloride (BAN)|Naphazoline hydrochloride (JP16/USP)|Tetrahydrozoline nitrate (JAN)|Orphenadrine citrate (USP)|Benztropine mesilate (JAN)|Biperiden (JAN/USP/INN)|Procyclidine hydrochloride (USP)|Trihexyphenidyl hydrochloride (JP16/USP)|Chlorpromazine hydrochloride (JP16/USP)|Epinephrine hydrochloride (JAN)|Tolazoline hydrochloride (JAN/USP)|Acetylcholine chloride (JP16/USP/INN)|Bethanechol chloride (JP16/USP)|Cyclopentolate hydrochloride (JP16/USP)|Hexocyclium metilsulfate (INN)|Homatropine hydrobromide (JP16/USP)|Isopropamide iodide (JAN/USP/INN)|Oxyphencyclimine hydrochloride (JAN)|Propiverine hydrochloride (JP16)|Dipivefrin hydrochloride (JAN/USP)|Metaraminol bitartrate (JAN/USP)|Methoxamine hydrochloride (JAN)|Naphazoline nitrate (JP16)|Oxymetazoline hydrochloride (JAN/USP)|Tetrahydrozoline hydrochloride (JAN/USP)|Tamsulosin hydrochloride (JP16/USAN)|Levobunolol hydrochloride (JAN/USP)|Atropine methonitrate (JAN/INN)|Trospium chloride (JAN/USAN/INN)|Profenamine hydrochloride (JAN)|Tolterodine tartrate (JAN/USAN)|Piperidolate hydrochloride (JAN)|Carpronium chloride (JAN/INN)|Alprenolol hydrochloride (JP16/USAN)|Tiemonium iodide (JAN/INN)|Piroheptine hydrochloride (JAN)|Ritodrine hydrochloride (JP16/USP)|Solifenacin succinate (JAN/USAN/INN)|Midodrine hydrochloride (JAN/USAN)|Methylbenactyzium bromide (JP16/INN)|Azosemide (JAN/USAN/INN)|Urapidil (JP16/INN)|Tramazoline hydrochloride (JAN/USAN)|Pirbuterol hydrochloride (JAN/USAN)|Mianserin hydrochloride (JAN/USAN)|Etomidoline (JAN/INN)|Clenbuterol hydrochloride (JAN/USP)|Tulobuterol hydrochloride (JP16)|Bevantolol hydrochloride (JAN/USAN)|Formoterol fumarate (USAN)|Prifinium bromide (JAN/INN)|Ephedrine hydrochloride (JP16/USP)|dl-Isoprenaline hydrochloride (JAN)|Norfenefrine hydrochloride (JAN)|Fenoterol hydrobromide (JAN)|Bunitrolol hydrochloride (JAN)|Scopolamine butylbromide (JP16)|Bupranolol hydrochloride (JP16)|Diponium bromide (JAN/INN)|Amosulalol hydrochloride (JP16)|Esatenolol (JAN/INN)|Butropium bromide (JP16/INN)|Trimebutine maleate (JP16)|Bufetolol hydrochloride (JP16)|Befunolol hydrochloride (JAN)|Levomepromazine hydrochloride (JAN/USAN)|Pipethanate hydrochloride (JAN)|Valethamate bromide (JAN)|Nylidrin hydrochloride (JAN)|Moxisylyte hydrochloride (JAN)|Etilefrine hydrochloride (JP16)|Mabuterol hydrochloride (JAN)|Diphenylpiperidinomethyldioxolan iodide (JAN)|Piretanide (JAN/USAN/INN)|Methoxyphenamine hydrochloride (JAN)|Hyoscyamine methylbromide (JAN)|Naftopidil (JAN/INN)|Nipradilol (JAN/INN)|Alfuzosin hydrochloride (JAN/USAN)|Darifenacin hydrobromide (JAN/USAN)|Celiprolol hydrochloride (JAN/USAN)|Isoxsuprine hydrochloride (JP16/USP)|Bopindolol malonate (JAN)|Oxprenolol hydrochloride (JP16/USP)|Oxapium iodide (JP16/INN)|Arotinolol hydrochloride (JP16)|Landiolol hydrochloride (JAN)|Metixene hydrochloride (JAN)|Tiquizium bromide (JAN/INN)|Bunazosin hydrochloride (JP16)|Tiotropium bromide hydrate (JAN)|Oxitropium bromide (JAN/INN)|L-Methylephedrine hydrochloride (JAN)|Aclatonium napadisilate (JAN)|Silodosin (JAN/INN)|N-Methylscopolamine methylsulfate (JAN)|Trimetoquinol hydrochloride|Pipethanate ethobromide (JAN)|Setiptiline maleate (JAN)|Isoprenaline sulfate (JAN)|Atropine sulfate (JP16/USP)|Homatropine methylbromide (USP)|Scopolamine hydrobromide hydrate (JP16)|Metipranolol hydrochloride|Isoetharine hydrochloride (USP)|dl-Methylephedrine hydrochloride (JP16)|Albuterol (USP)|Epinephrine bitartrate (JAN/USP)|l-Isoprenaline hydrochloride (JP16)|Tulobuterol (JAN/INN)|Pilocarpine hydrochloride (JP16/USP)|Dihydroergotamine mesilate (JP16)|Ipratropium bromide hydrate (JP16)|Biperiden hydrochloride (JP16/USP)|Biperiden lactate (JAN/USP)|Levomepromazine maleate (JP16/USAN)|Levalbuterol hydrochloride (USAN)|Acebutolol (USAN/INN)|Bisoprolol (JAN/USAN/INN)|Dipivefrin (USAN)|Metoprolol (USAN/INN)|Ritodrine (USAN/INN)|Ketanserin (USAN/INN)|Metipranolol (USAN/INN)|Primidolol (USAN/INN)|Hexoprenaline sulfate (USAN)|Flutropium bromide (JAN)|Timepidium bromide hydrate (JP16)|Orphenadrine hydrochloride|Denopamine (JAN/INN)|Talibegron hydrochloride (USAN)|Alprenoxime hydrochloride (USAN)|Alvameline maleate (USAN)|Arbutamine hydrochloride (USAN)|Arformoterol tartrate (USAN)|Asenapine maleate (USAN)|Atropine oxide hydrochloride (USAN)|Bucindolol hydrochloride (USAN)|Bunolol hydrochloride (USAN)|Butopamine (USAN/INN)|Butoxamine hydrochloride (USAN)|Mazaticol hydrochloride hydrate (JAN)|Chlorpromazine hibenzate (JAN)|Profenamine hibenzate (JAN)|Carbuterol hydrochloride (USAN)|Carvedilol phosphate hydrate (JAN)|Cetamolol hydrochloride (USAN)|Cicloprolol hydrochloride (USAN)|Cimaterol (USAN/INN)|Colterol mesylate (USAN)|Dapiprazole hydrochloride (USAN)|Darifenacin (USAN/INN)|Dexetimide (USAN/INN)|Dexpropranolol hydrochloride (USAN)|Diacetolol hydrochloride (USAN)|Atropine methylbromide (JAN)|Dobutamine (USP/INN)|Dobutamine lactobionate (USAN)|Dobutamine tartrate (USP)|Dopexamine (USAN/INN)|Ephedrine sulfate (USP)|Chlorpromazine phenolphthalinate (JAN)|Esoxybutynin chloride (USAN)|Ethybenztropine (USAN)|Eucatropine hydrochloride (USP XXXII)|Fenoterol (USAN/INN)|Fiduxosin hydrochloride (USAN)|Flestolol sulfate (USAN)|Hyoscyamine hydrobromide (USP)|Indoramin (USAN/INN)|Indoramin hydrochloride (USAN)|Isoetharine (USP)|Isoetharine mesylate (USP)|Levalbuterol tartrate (USAN)|Levdobutamine lactobionate (USAN)|Levobetaxolol hydrochloride (USAN)|Medroxalol (USAN/INN)|Medroxalol hydrochloride (USAN)|Metaproterenol polistirex (USAN)|Methacholine chloride (USAN/INN)|Metoprolol fumarate (USP)|Milameline hydrochloride (USAN)|Trimetoquinol hydrochloride hydrate (JP16)|Nebivolol (USAN/INN)|Norepinephrine bitartrate (USP)|Formoterol fumarate hydrate (JP16)|Pamatolol sulfate (USAN)|Procaterol hydrochloride hydrate (JP16)|Pelanserin hydrochloride (USAN)|Picumeterol fumarate (USAN)|Pilocarpine nitrate (USP)|Practolol (USAN)|Prenalterol hydrochloride (USAN)|Pseudoephedrine polistirex (USAN)|Pseudoephedrine sulfate (USP)|Reproterol hydrochloride (USAN)|Rimiterol hydrobromide (USAN)|Salmeterol (USAN/INN)|Sibenadet hydrochloride (USAN)|Solabegron hydrochloride (USAN)|Imidafenacin (JAN/INN)|Xamoterol (USAN)|Xamoterol fumarate (USAN)|Nebivolol hydrochloride (USAN)|Olanzapine pamoate (USAN)|Epanolol (USAN/INN)|Cimetropium bromide (INN)|Alfuzosin (INN)|Oxedrine (BAN)|Alprenolol (INN)|Mepindolol (INN)|Tertatolol (INN)|Cloranolol (INN)|Talinolol (INN)|Choline alfoscerate (INN)|Bambuterol (INN)|Amosulalol (INN)|Arformoterol (INN)|Arotinolol (INN)|Atropine oxide (INN)|Bambuterol hydrocloride|Benzatropine (INN)|Betaxolol (INN)|Bitolterol (INN)|Bopindolol (INN)|Bunazosin (INN)|Buphenine (INN)|Bupranolol (INN)|Carazolol (INN)|Carteolol (INN)|Celiprolol (INN)|Cevimeline (INN)|Clenbuterol (INN)|Cyclopentolate (INN)|Dihydroergotamine (INN)|Dihydroergotamine tartrate|Doxazosin (INN)|Ergometrine (INN)|Ergotamine (INN)|Esmolol (INN)|Etilefrine (INN)|Fentonium bromide (INN)|Formoterol (INN)|Hexoprenaline (INN)|Penbutolol (INN)|Isoprenaline (INN)|Isoxsuprine (INN)|Isoxsuprine lactate|Ketanserin tartrate|Labetalol (INN)|Levobunolol (INN)|Levosalbutamol (INN)|Mazaticol (INN)|Metaraminol (INN)|Methylephedrine (BAN)|Methylergometrine (INN)|Mianserin (INN)|Midodrine (INN)|Moxisylyte (INN)|Naphazoline (INN)|Norepinephrine hydrochoride|Norfenefrine (INN)|Orciprenaline (INN)|Orphenadrine (INN)|Oxedrine tartrate|Oxedrine hydrochloride|Oxprenolol (INN)|Oxymetazoline (INN)|Oxyphencyclimine (INN)|Phenoxybenzamine (INN)|Phentolamine (INN)|Phenylephrine (INN)|Phenylephrine tartrate|Pilocarpine borate|Piperidolate (INN)|Pipethanate (INN)|Pirbuterol (INN)|Piroheptine (INN)|Prazosin (INN)|Procaterol (INN)|Procyclidine (INN)|Profenamine (INN)|Propiverine (INN)|Propranolol (INN)|Pseudoephedrine (INN)|Quetiapine (INN)|Reproterol (INN)|Setiptiline (INN)|Solifenacin (INN)|Tamsulosin (INN)|Terazosin (INN)|Terbutaline (INN)|Tertatolol hydrochloride|Tetryzoline (INN)|Tiemonium methylsulfate|Timolol (INN)|Tolazoline (INN)|Tramazoline (INN)|Tretoquinol (INN)|Trihexyphenidyl (INN)|Trimebutine (INN)|Urapidil hydrochloride|Phenylephrine bitartrate (USP)|Indacaterol (USAN/INN)|Indacaterol maleate (JAN/USAN)|Mirabegron (USAN/JAN)|Ritobegron ethyl hydrochloride (JAN)|Carpronium chloride hydrate (JAN)|Norepinephrine hydrochloride (JAN)|Olodaterol hydrochloride (JAN/USAN)	Saliva has manifold functions in maintaining the integrity of the oral tissues, in protecting teeth from caries, in the tasting and ingestion of food, in speech and in the tolerance of tenures, for example. Salivary secretion occurs in response to stimulation by neurotransmitters released from autonomic nerve endings. There are two secretory pathways: protein exocytosis and fluid secretion. Sympathetic stimulation leads to the activation of adenylate cyclase and accumulation of intracellular cAMP. The elevation of cAMP causes the secretion of proteins such as amylase and mucin. In contrast, parasympathetic stimulation activates phospholipase C and causes the elevation of intracellular Ca2+, which leads to fluid secretion; that is, water and ion transport. Ca2+ also induces amylase secretion, but the amount is smaller than that induced by cAMP.
hsa04070	Phosphatidylinositol signaling system - Homo sapiens (human)	Environmental Information Processing; Signal Transduction	5298:PI4KB|5297:PI4KA|55361:PI4K2A|55300:PI4K2B|8394:PIP5K1A|8395:PIP5K1B|23396:PIP5K1C|8525:DGKZ|1607:DGKB|1609:DGKQ|1608:DGKG|9162:DGKI|8527:DGKD|1606:DGKA|8526:DGKE|160851:DGKH|3706:ITPKA|3707:ITPKB|3705:ITPK1|5289:PIK3C3|5305:PIP4K2A|8396:PIP4K2B|79837:PIP4K2C|200576:PIKFYVE|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|5288:PIK3C2G|5287:PIK3C2B|5286:PIK3C2A|64768:IPPK|1040:CDS1|8760:CDS2|10423:CDIPT|3612:IMPA1|3613:IMPA2|8871:SYNJ2|3633:INPP5B|56623:INPP5E|8867:SYNJ1|4952:OCRL|5728:PTEN|3636:INPPL1|3632:INPP5A|27124:INPP5J|51763:INPP5K|3628:INPP1|4534:MTM1|8821:INPP4B|3631:INPP4A|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|84812:PLCD4|113026:PLCD3|5333:PLCD1|51196:PLCE1|5335:PLCG1|5336:PLCG2|89869:PLCZ1|3708:ITPR1|3709:ITPR2|3710:ITPR3|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5579:PRKCB|5578:PRKCA|5582:PRKCG|3635:INPP5D|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|54928:IMPAD1	Joubert syndrome|Lowe syndrome|Dent disease|Centronuclear myopathy|Lethal congenital contractural syndrome (LCCS)|Fleck corneal dystrophy (FCD)|VACTERL/VATER association		
hsa00062	Fatty acid elongation - Homo sapiens (human)	Metabolism; Lipid Metabolism	10449:ACAA2|3032:HADHB|3033:HADH|3030:HADHA|1892:ECHS1|51102:MECR|9374:PPT2|5538:PPT1|64834:ELOVL1|54898:ELOVL2|83401:ELOVL3|6785:ELOVL4|60481:ELOVL5|79071:ELOVL6|79993:ELOVL7|51144:HSD17B12|201562:PTPLB|9200:PTPLA|9524:TECR|122970:ACOT4|641371:ACOT1|10965:ACOT2|11332:ACOT7	Neuronal ceroid lipofuscinosis|Hyperargininemia|Progressive myoclonic epilepsy (PME)|Stargardt disease (STGD)		
hsa00730	Thiamine metabolism - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	9054:NFS1|84284:NTPCR|27010:TPK1|79178:THTPA			
hsa03460	Fanconi anemia pathway - Homo sapiens (human)	Genetic Information Processing; Replication and Repair	84126:ATRIP|545:ATR|57697:FANCM|91442:C19orf40|378708:APITD1|201254:STRA13|9894:TELO2|3280:HES1|80233:C17orf70|2175:FANCA|2187:FANCB|2176:FANCC|2178:FANCE|2188:FANCF|2189:FANCG|55120:FANCL|57599:WDR48|7398:USP1|29089:UBE2T|55215:FANCI|2177:FANCD2|675:BRCA2|79728:PALB2|5889:RAD51C|5888:RAD51|672:BRCA1|83990:BRIP1|22909:FAN1|4292:MLH1|5395:PMS2|51455:REV1|5980:REV3L|51426:POLK|5429:POLH|11201:POLI|80010:RMI1|116028:RMI2|7156:TOP3A|8940:TOP3B|641:BLM|6117:RPA1|6118:RPA2|6119:RPA3|29935:RPA4|80198:MUS81|146956:EME1|197342:EME2|2072:ERCC4|2067:ERCC1|79008:SLX1B|548593:SLX1A|84464:SLX4	Fanconi anemia|Seckel syndrome		The Fanconi anemia pathway is required for the efficient repair of damaged DNA, especially interstrand cross-links (ICLs). DNA ICL is directly recognized by FANCM and associated proteins, that recruit the FA core complex. The FA core complex monoubiquitinates FANCD2 and FANCI. The monoubiquitinated FANCD2/FANCI becomes an active form and interacts with a series of DNA repair proteins and facilitates downstream repair pathways. Fanconi anemia is caused by mutations in one of at least 13 FA genes and is characterized by congenital growth abnormalities, bone marrow failure and cancer predisposition.
hsa04910	Insulin signaling pathway - Homo sapiens (human)	Organismal Systems; Endocrine System	3630:INS|3643:INSR|8471:IRS4|8660:IRS2|3667:IRS1|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|5170:PDPK1|207:AKT1|208:AKT2|10000:AKT3|2932:GSK3B|2997:GYS1|2998:GYS2|5501:PPP1CC|5499:PPP1CA|5500:PPP1CB|5507:PPP1R3C|5509:PPP1R3D|79660:PPP1R3B|5506:PPP1R3A|5261:PHKG2|5260:PHKG1|5256:PHKA2|5257:PHKB|5255:PHKA1|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|5837:PYGM|5834:PYGB|5836:PYGL|5140:PDE3B|5139:PDE3A|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|5573:PRKAR1A|5577:PRKAR2B|5576:PRKAR2A|5575:PRKAR1B|3991:LIPE|5584:PRKCI|5590:PRKCZ|6517:SLC2A4|2319:FLOT2|10211:FLOT1|10603:SH2B2|10580:SORBS1|23624:CBLC|868:CBLB|867:CBL|1399:CRKL|1398:CRK|2889:RAPGEF1|23433:RHOQ|23265:EXOC7|9322:TRIP10|6720:SREBF1|31:ACACA|32:ACACB|2194:FASN|5313:PKLR|3101:HK3|3099:HK2|3098:HK1|80201:HKDC1|2645:GCK|5562:PRKAA1|5563:PRKAA2|5565:PRKAB2|5564:PRKAB1|5571:PRKAG1|53632:PRKAG3|51422:PRKAG2|2308:FOXO1|10891:PPARGC1A|2538:G6PC|57818:G6PC2|8789:FBP2|2203:FBP1|5106:PCK2|5105:PCK1|2475:MTOR|57521:RPTOR|6199:RPS6KB2|6198:RPS6KB1|6194:RPS6|1978:EIF4EBP1|9470:EIF4E2|1977:EIF4E|253314:EIF4E1B|7248:TSC1|7249:TSC2|6009:RHEB|572:BAD|25759:SHC2|6464:SHC1|53358:SHC3|399694:SHC4|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|8569:MKNK1|2872:MKNK2|2002:ELK1|8651:SOCS1|8835:SOCS2|9021:SOCS3|122809:SOCS4|5770:PTPN1|5792:PTPRF|5602:MAPK10|5601:MAPK9|5599:MAPK8|3551:IKBKB|51763:INPP5K|3636:INPPL1	Glycogen storage diseases (GSD)|Maturity onset diabetes of the young (MODY)|Familial partial lipodystrophy (FPL)|Permanent neonatal diabetes mellitus (PNDM)|Leprechaunism |Lymphangioleiomyomatosis (LAM)|Tuberous sclerosis complex (TSC)|Rabson-Mendenhall syndrome|Pituitary adenomas|Wolff-Parkinson-White (WPW) syndrome	Insulin (JAN/USP)|Amrinone (JAN/INN)|Dipyridamole (JP16/USP/INN)|Milrinone (JAN/USP/INN)|Buformin (USAN/INN)|Metformin hydrochloride (JP16/USP)|Pimobendan (JAN/USAN/INN)|Vesnarinone (JAN/USAN/INN)|Proxyphylline (JAN/INN)|Cilostazol (JP16/USAN/INN)|Olprinone hydrochloride hydrate (JAN)|Inamrinone lactate|Milrinone lactate|Buformin hydrochloride (JP16)|Insulin human (genetical recombination) (JP16)|Insulin glargine (genetical recombination) (JAN)|Dapiclermin (USAN/INN)|Enoximone (USAN/INN)|Insulin aspart (genetical recombination) (JAN)|Insulin lispro (genetical recombination) (JAN)|Imazodan hydrochloride (USAN)|Indolidan (USAN/INN)|Ingliforib (USAN/INN)|Insulin detemir (genetical recombination) (JAN)|Insulin glulisine (genetical recombination) (JAN)|Insulin human, isophane (USP)|Insulin human zinc (USP)|Insulin human zinc, extended (USP)|Insulin I 125 (USAN)|Insulin I 131 (USAN)|Insulin, dalanated (USAN)|Isophane insulin injection (aqueous suspension) (JAN)|Insulin, neutral (USAN)|Insulin zinc, extended (USP)|Insulin zinc, prompt (USP)|Insulin zinc (USP)|Isomazole hydrochloride (USAN)|Levosimendan (USAN/INN)|Lixazinone sulfate (USAN)|Metformin (USAN/INN)|Aminophylline hydrate (JP16)|Proinsulin human (USAN)|Insulin injection, biphasic isophane (BAN)|Insulin degludec (genetical recombination) (JAN)	Insulin binding to its receptor results in the tyrosine phosphorylation of insulin receptor substrates (IRS) by the insulin receptor tyrosine kinase (INSR). This allows association of IRSs with the regulatory subunit of phosphoinositide 3-kinase (PI3K). PI3K activates 3-phosphoinositide-dependent protein kinase 1 (PDK1), which activates Akt, a serine kinase. Akt in turn deactivates glycogen synthase kinase 3 (GSK-3), leading to activation of glycogen synthase (GYS) and thus glycogen synthesis. Activation of Akt also results in the translocation of GLUT4 vesicles from their intracellular pool to the plasma membrane, where they allow uptake of glucose into the cell. Akt also leads to mTOR-mediated activation of protein synthesis by eIF4 and p70S6K. The translocation of GLUT4 protein is also elicited through the CAP/Cbl/TC10 pathway, once Cbl is phosphorylated by INSR.|Other signal transduction proteins interact with IRS including GRB2. GRB2 is part of the cascade including SOS, RAS, RAF and MEK that leads to activation of mitogen-activated protein kinase (MAPK) and mitogenic responses in the form of gene transcription. SHC is another substrate of INSR. When tyrosine phosphorylated, SHC associates with GRB2 and can thus activate the RAS/MAPK pathway independently of IRS-1.
hsa05016	Huntington's disease - Homo sapiens (human)	Human Diseases; Neurodegenerative Diseases	1211:CLTA|1212:CLTB|8218:CLTCL1|1213:CLTC|3092:HIP1|161:AP2A2|160:AP2A1|163:AP2B1|1173:AP2M1|1175:AP2S1|3064:HTT|55081:IFT57|841:CASP8|836:CASP3|2911:GRM1|2915:GRM5|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|2902:GRIN1|2904:GRIN2B|3708:ITPR1|1742:DLG4|7052:TGM2|5978:REST|25942:SIN3A|23186:RCOR1|3066:HDAC2|3065:HDAC1|5430:POLR2A|5431:POLR2B|5432:POLR2C|5433:POLR2D|5434:POLR2E|5435:POLR2F|5436:POLR2G|5437:POLR2H|5438:POLR2I|5441:POLR2L|5439:POLR2J|246721:POLR2J2|548644:POLR2J3|5440:POLR2K|627:BDNF|1639:DCTN1|10540:DCTN2|51164:DCTN4|9001:HAP1|25981:DNAH1|55567:DNAH3|146754:DNAH2|7802:DNALI1|27019:DNAI1|64446:DNAI2|83544:DNAL1|10126:DNAL4|1387:CREBBP|2033:EP300|6874:TAF4|6875:TAF4B|387332:TBPL2|9519:TBPL1|6908:TBP|6667:SP1|1385:CREB1|10488:CREB3|64764:CREB3L2|84699:CREB3L3|148327:CREB3L4|90993:CREB3L1|9586:CREB5|10891:PPARGC1A|5468:PPARG|7019:TFAM|4899:NRF1|6647:SOD1|6648:SOD2|7350:UCP1|7157:TP53|581:BAX|27113:BBC3|4723:NDUFV1|4729:NDUFV2|4731:NDUFV3|4694:NDUFA1|4695:NDUFA2|4696:NDUFA3|4697:NDUFA4|56901:NDUFA4L2|4698:NDUFA5|4700:NDUFA6|4701:NDUFA7|4702:NDUFA8|4704:NDUFA9|4705:NDUFA10|4706:NDUFAB1|126328:NDUFA11|55967:NDUFA12|51079:NDUFA13|4707:NDUFB1|4708:NDUFB2|4709:NDUFB3|4710:NDUFB4|4711:NDUFB5|4712:NDUFB6|4713:NDUFB7|4714:NDUFB8|4715:NDUFB9|4716:NDUFB10|54539:NDUFB11|4719:NDUFS1|4720:NDUFS2|4722:NDUFS3|4724:NDUFS4|4725:NDUFS5|4726:NDUFS6|374291:NDUFS7|4728:NDUFS8|4717:NDUFC1|4718:NDUFC2|6389:SDHA|6390:SDHB|6391:SDHC|6392:SDHD|7386:UQCRFS1|4519:CYTB|1537:CYC1|7384:UQCRC1|7385:UQCRC2|7388:UQCRH|440567:UQCRHL|7381:UQCRB|27089:UQCRQ|29796:UQCR10|10975:UQCR11|4514:COX3|4512:COX1|4513:COX2|1327:COX4I1|84701:COX4I2|9377:COX5A|1329:COX5B|1337:COX6A1|1339:COX6A2|1340:COX6B1|125965:COX6B2|1345:COX6C|1347:COX7A2|1346:COX7A1|9167:COX7A2L|1349:COX7B|170712:COX7B2|1350:COX7C|1351:COX8A|341947:COX8C|498:ATP5A1|506:ATP5B|509:ATP5C1|513:ATP5D|514:ATP5E|4508:ATP6|515:ATP5F1|518:ATP5G3|516:ATP5G1|517:ATP5G2|10476:ATP5H|539:ATP5O|522:ATP5J|4509:ATP8|7416:VDAC1|7417:VDAC2|7419:VDAC3|292:SLC25A5|293:SLC25A6|291:SLC25A4|83447:SLC25A31|54205:CYCS|317:APAF1|842:CASP9|2876:GPX1|100532726:NDUFC2-KCTD14|10105:PPIF	Huntington's disease (HD)|Mitochondrial respiratory chain deficiencies (MRCD)		Huntington disease (HD) is an autosomal-dominant neurodegenerative disorder that primarily affects medium spiny striatal neurons (MSN). The symptoms are choreiform, involuntary movements, personality changes and dementia. HD is caused by a CAG repeat expansion in the IT15gene, which results in a long stretch of polyglutamine close to the amino-terminus of the HD protein huntingtin (Htt). Mutant Htt (mHtt) has effects both in the cytoplasm and in the nucleus. In the cytoplasm, full-length mHtt can interfere with BDNF vesicular transport on microtubules. This mutant protein also may lead to abnormal endocytosis and secretion in neurons, because normal Htt form a complex with the proteins Hip1, clathrin and AP2 that are involved in endocytosis. In addition, mHtt affects Ca2+ signaling by sensitizing InsP3R1 to activation by InsP3, stimulating NMDAR activity, and destabilizing mitochondrial Ca2+ handling. The mHtt translocates to the nucleus, where it forms intranuclear inclusions. Nuclear toxicity is believed to be caused by interference with gene transcription, leading to loss of transcription of neuroprotective molecules such as BDNF. While mHtt binds to p53 and upregulates levels of nuclear p53 as well as p53 transcriptional activity. Augmented p53 mediates mitochondrial dysfunction.
hsa04141	Protein processing in endoplasmic reticulum - Homo sapiens (human)	Genetic Information Processing; Folding, Sorting and Degradation	55176:SEC61A2|29927:SEC61A1|10952:SEC61B|23480:SEC61G|7095:SEC62|11231:SEC63|6184:RPN1|6185:RPN2|1603:DAD1|7991:TUSC3|1650:DDOST|3703:STT3A|201595:STT3B|7841:MOGS|10970:CKAP4|6238:RRBP1|64374:SIL1|10525:HYOU1|3309:HSPA5|51726:DNAJB11|64215:DNAJC1|5611:DNAJC3|54431:DNAJC10|7184:HSP90B1|23193:GANAB|5589:PRKCSH|821:CANX|2923:PDIA3|811:CALR|57134:MAN1C1|4121:MAN1A1|10905:MAN1A2|11253:MAN1B1|10960:LMAN2|3998:LMAN1|79748:LMAN1L|10113:PREB|56681:SAR1A|51128:SAR1B|6396:SEC13|25956:SEC31B|22872:SEC31A|10484:SEC23A|10483:SEC23B|9632:SEC24C|9871:SEC24D|10802:SEC24A|10427:SEC24B|55757:UGGT2|56886:UGGT1|9695:EDEM1|55741:EDEM2|80267:EDEM3|5034:P4HB|9601:PDIA4|10130:PDIA6|10961:ERP29|81567:TXNDC5|30001:ERO1L|56605:ERO1LB|10956:OS9|27248:ERLEC1|6745:SSR1|6746:SSR2|6747:SSR3|6748:SSR4|10134:BCAP31|23471:TRAM1|79139:DERL1|51009:DERL2|91319:DERL3|80700:UBXN6|55968:NSFL1C|258010:SVIP|7415:VCP|55666:NPLOC4|7353:UFD1L|3306:HSPA2|3310:HSPA6|3304:HSPA1B|3305:HSPA1L|3312:HSPA8|3303:HSPA1A|3301:DNAJA1|10294:DNAJA2|3337:DNAJB1|3300:DNAJB2|54788:DNAJB12|85479:DNAJC5B|80331:DNAJC5|285126:DNAJC5G|3320:HSP90AA1|3326:HSP90AB1|22824:HSPA4L|10808:HSPH1|573:BAG1|9532:BAG2|23640:HSPBP1|1409:CRYAA|1410:CRYAB|55432:YOD1|9373:PLAA|5887:RAD23B|5886:RAD23A|56893:UBQLN4|29979:UBQLN1|50613:UBQLN3|29978:UBQLN2|143630:UBQLNL|55768:NGLY1|92552:ATXN3L|4287:ATXN3|10277:UBE4B|5610:EIF2AK2|27102:EIF2AK1|440275:EIF2AK4|9451:EIF2AK3|1965:EIF2S1|4780:NFE2L2|468:ATF4|23645:PPP1R15A|1649:DDIT3|596:BCL2|22926:ATF6|1388:ATF6B|7466:WFS1|8720:MBTPS1|51360:MBTPS2|7494:XBP1|2081:ERN1|7186:TRAF2|4217:MAP3K5|5609:MAP2K7|5602:MAPK10|5601:MAPK9|5599:MAPK8|581:BAX|578:BAK1|823:CAPN1|824:CAPN2|10299:MARCH6|51465:UBE2J1|118424:UBE2J2|7326:UBE2G1|7327:UBE2G2|84447:SYVN1|6048:RNF5|91445:RNF185|55829:SELS|6400:SEL1L|9709:HERPUD1|267:AMFR|10273:STUB1|7325:UBE2E2|7324:UBE2E1|7323:UBE2D3|7322:UBE2D2|7321:UBE2D1|10477:UBE2E3|51619:UBE2D4|5071:PARK2|9978:RBX1|8454:CUL1|6500:SKP1|26232:FBXO2|26270:FBXO6	Frontotemporal lobar degeneration (FTLD)|Combined deficiency of factors V and VIII (F5F8D)|Leprosy|Polycystic liver disease|Distal muscular dystrophies|Myofibrillar myopathies (MFM)|Ichthyosis follicularis, alopecia, and photophobia syndrome|Wolcott-Rallison syndrome|Nonsyndromic autosomal recessive mental retardation (NS-ARMR)|Wolfram syndrome (WFS)|Congenital dyserythropoietic anemias (CDAs)|Chylomicron retention disease (CRD)|Cranio-lenticulo-sutural dysplasia (CLSD)		The endoplasmic reticulum (ER) is a subcellular organelle where proteins are folded with the help of lumenal chaperones. Newly synthesized peptides enter the ER via the sec61 pore and are glycosylated. Correctly folded proteins are packaged into transport vesicles that shuttle them to the Golgi complex. Misfolded proteins are retained within the ER lumen in complex with molecular chaperones. Proteins that are terminally misfolded bind to BiP and are directed toward degradation through the proteasome in a process called ER-associated degradation (ERAD). Accumulation of misfolded proteins in the ER causes ER stress and activates a signaling pathway called the unfolded protein response (UPR). In certain severe situations, however, the protective mechanisms activated by the UPR are not sufficient to restore normal ER function and cells die by apoptosis.
hsa04662	B cell receptor signaling pathway - Homo sapiens (human)	Organismal Systems; Immune System	100132941:uncharacterized|100291917:uncharacterized|973:CD79A|974:CD79B|4067:LYN|6850:SYK|695:BTK|27071:DAPP1|29760:BLNK|10451:VAV3|7409:VAV1|7410:VAV2|5879:RAC1|5880:RAC2|5881:RAC3|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|4776:NFATC4|4772:NFATC1|4773:NFATC2|4775:NFATC3|10725:NFAT5|2885:GRB2|6654:SOS1|6655:SOS2|25780:RASGRP3|3265:HRAS|3845:KRAS|4893:NRAS|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|2353:FOS|3725:JUN|84433:CARD11|8915:BCL10|10892:MALT1|1147:CHUK|3551:IKBKB|8517:IKBKG|4790:NFKB1|5970:RELA|4792:NFKBIA|4793:NFKBIB|4794:NFKBIE|975:CD81|930:CD19|1380:CR2|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|207:AKT1|208:AKT2|10000:AKT3|2932:GSK3B|3635:INPP5D|933:CD22|971:CD72|5777:PTPN6|118788:PIK3AP1|11025:LILRB3|2213:FCGR2B|5336:PLCG2|5579:PRKCB|8519:IFITM1|3636:INPPL1	Osteoporosis, lymphedema, anhydrotic ectodermal dysplasia with immunodeficiency (OLEDAID)|Incontinentia pigmenti|Cocoon syndrome	Epratuzumab (USAN/INN)	B cells are an important component of adaptive immunity. They produce and secrete millions of different antibody molecules, each of which recognizes a different (foreign) antigen. The B cell receptor (BCR) is an integral membrane protein complex that is composed of two immunoglobulin (Ig) heavy chains, two Ig light chains and two heterodimers of Ig-alpha and Ig-beta. After BCR ligation by antigen, three main protein tyrosine kinases (PTKs) -the SRC-family kinase LYN, SYK and the TEC-family kinase BTK- are activated. Phosphatidylinositol 3-kinase (PI3K) and phospholipase C-gamma 2 (PLC-gamma 2) are important downstream effectors of BCR signalling. This signalling ultimately results in the expression of immediate early genes that further activate the expression of other genes involved in B cell proliferation, differentiation and Ig production as well as other processes.
hsa05032	Morphine addiction - Homo sapiens (human)	Human Diseases; Substance Dependence	10681:GNB5|107:ADCY1|108:ADCY2|10846:PDE10A|109:ADCY3|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|134:ADORA1|140679:SLC32A1|156:ADRBK1|157:ADRBK2|1812:DRD1|196883:ADCY4|200959:GABRR3|2550:GABBR1|2554:GABRA1|2555:GABRA2|2556:GABRA3|2557:GABRA4|2558:GABRA5|2559:GABRA6|2560:GABRB1|2561:GABRB2|2562:GABRB3|2563:GABRD|2564:GABRE|2565:GABRG1|2566:GABRG2|2567:GABRG3|2568:GABRP|2569:GABRR1|2570:GABRR2|27115:PDE7B|2770:GNAI1|2771:GNAI2|2773:GNAI3|2775:GNAO1|2778:GNAS|2782:GNB1|2783:GNB2|2784:GNB3|2785:GNG3|2786:GNG4|2787:GNG5|2788:GNG7|2790:GNG10|2791:GNG11|2792:GNGT1|2793:GNGT2|2868:GRK4|2869:GRK5|2870:GRK6|3760:KCNJ3|3762:KCNJ5|3763:KCNJ6|3765:KCNJ9|408:ARRB1|409:ARRB2|4988:OPRM1|50940:PDE11A|5136:PDE1A|5137:PDE1C|5138:PDE2A|5139:PDE3A|5140:PDE3B|5141:PDE4A|5142:PDE4B|5143:PDE4C|5144:PDE4D|5150:PDE7A|5151:PDE8A|5153:PDE1B|51764:GNG13|54331:GNG2|5566:PRKACA|5567:PRKACB|5568:PRKACG|5578:PRKCA|5579:PRKCB|5582:PRKCG|55879:GABRQ|55970:GNG12|5613:PRKX|59345:GNB4|773:CACNA1A|774:CACNA1B|8622:PDE8B|94235:GNG8|9568:GABBR2			Morphine is an alkaloid from the plant extracts of opium poppy. Although morphine is highly effective for the treatment of pain, it is also known to be intensely addictive. We now know that the most important brain-reward circuit involves dopamine (DA) -containing neurons in the ventral tegmental area (VTA) of the midbrain and their target areas in the limbic forebrain, in particular, the nucleus accumbens (NAc) and frontal regions of cerebral cortex. Morphine can cause indirect excitation of VTA dopamine neurons by reducing inhibitory synaptic transmission mediated by GABAergic neurons. The chronic use of morphine is characterized by adaptive changes in neurons and neuronal communication;  such adaptations (e.g., 'superactivation' of adenylyl cyclase) must underlie altered behaviour associated with morphine dependence and withdrawal syndrome, as well as drug-induced craving and relapse to drug use.
hsa00480	Glutathione metabolism - Homo sapiens (human)	Metabolism; Metabolism of Other Amino Acids	2678:GGT1|2686:GGT7|2687:GGT5|124975:GGT6|79017:GGCT|26873:OPLAH|2729:GCLC|2730:GCLM|2937:GSS|51056:LAP3|290:ANPEP|4257:MGST1|4258:MGST2|2940:GSTA3|2939:GSTA2|2946:GSTM2|2941:GSTA4|2948:GSTM4|2953:GSTT2|2949:GSTM5|2947:GSTM3|9446:GSTO1|4259:MGST3|119391:GSTO2|2938:GSTA1|2952:GSTT1|2944:GSTM1|2950:GSTP1|221357:GSTA5|373156:GSTK1|2936:GSR|3418:IDH2|3417:IDH1|5226:PGD|2539:G6PD|51060:TXNDC12|2882:GPX7|2880:GPX5|2877:GPX2|2878:GPX3|2876:GPX1|257202:GPX6|2879:GPX4|4953:ODC1|6723:SRM|6611:SMS|6240:RRM1|6241:RRM2|50484:RRM2B	Snyder-Robinson syndrome|Anemia due to disorders of glutathione metabolism|Progressive external ophthalmoplegia (PEO)	Hydroxycarbamide (JAN/INN)|Gemcitabine hydrochloride (JAN/USAN)|Gemcitabine (USAN/INN)	
hsa00500	Starch and sucrose metabolism - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	8972:MGAM|2548:GAA|2595:GANC|6476:SI|57733:GBA3|11181:TREH|7358:UGDH|7363:UGT2B4|574537:UGT2A2|7367:UGT2B17|7365:UGT2B10|7364:UGT2B7|7366:UGT2B15|54577:UGT1A7|10720:UGT2B11|54490:UGT2B28|54579:UGT1A5|54659:UGT1A3|54657:UGT1A4|54578:UGT1A6|54576:UGT1A8|54600:UGT1A9|10941:UGT2A1|54575:UGT1A10|79799:UGT2A3|54658:UGT1A1|2990:GUSB|9365:KL|80146:UXS1|7360:UGP2|5236:PGM1|55276:PGM2|3101:HK3|3099:HK2|3098:HK1|80201:HKDC1|2645:GCK|2538:G6PC|57818:G6PC2|283209:PGM2L1|2821:GPI|2632:GBE1|5837:PYGM|5834:PYGB|5836:PYGL|2997:GYS1|2998:GYS2|277:AMY1B|276:AMY1A|278:AMY1C|280:AMY2B|279:AMY2A|178:AGL|5169:ENPP3|5167:ENPP1	Glycogen storage diseases (GSD)|Congenital sucrase-isomaltase deficiency|Generalized arterial calcification of infancy|Familial tumoral calcinosis (FTC)	Acarbose (JAN/USAN/INN)|Miglitol (JAN/USAN/INN)|Voglibose (JP16/USAN/INN)|Ingliforib (USAN/INN)	
hsa05100	Bacterial invasion of epithelial cells - Homo sapiens (human)	Human Diseases; Infectious Diseases	999:CDH1|1499:CTNNB1|1496:CTNNA2|1495:CTNNA1|29119:CTNNA3|79658:ARHGAP10|4233:MET|2549:GAB1|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|1399:CRKL|1398:CRK|1793:DOCK1|998:CDC42|5879:RAC1|7454:WAS|8976:WASL|8936:WASF1|10163:WASF2|10095:ARPC1B|10552:ARPC1A|10109:ARPC2|10094:ARPC3|10093:ARPC4|10092:ARPC5|81873:ARPC5L|60:ACTB|71:ACTG1|1731:SEPT1|23624:CBLC|868:CBLB|867:CBL|25759:SHC2|6464:SHC1|53358:SHC3|399694:SHC4|23607:CD2AP|26052:DNM3|1785:DNM2|10059:DNM1L|1759:DNM1|1211:CLTA|1212:CLTB|8218:CLTCL1|1213:CLTC|857:CAV1|858:CAV2|859:CAV3|3059:HCLS1|2017:CTTN|6714:SRC|5747:PTK2|9564:BCAR1|5829:PXN|2335:FN1|3678:ITGA5|3688:ITGB1|3611:ILK|10459:MAD2L2|26084:ARHGEF26|391:RHOG|9844:ELMO1|387:RHOA|7414:VCL			Many pathogenic bacteria can invade phagocytic and non-phagocytic cells and colonize them intracellularly, then become disseminated to other cells. Invasive bacteria induce their own uptake by non-phagocytic host cells (e.g. epithelial cells) using two mechanisms referred to as zipper model and trigger model. Listeria, Staphylococcus, Streptococcus, and Yersinia are examples of bacteria that enter using the zipper model. These bacteria express proteins on their surfaces that interact with cellular receptors, initiating signalling cascades that result in close apposition of the cellular membrane around the entering bacteria. Shigella and Salmonella are the examples of bacteria entering cells using the trigger model. These bacteria use type III secretion systems to inject protein effectors that interact with the actin cytoskeleton.
hsa04975	Fat digestion and absorption - Homo sapiens (human)	Organismal Systems; Digestive System	8513:LIPF|5406:PNLIP|5407:PNLIPRP1|5408:PNLIPRP2|1056:CEL|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|1208:CLPS|948:CD36|2806:GOT2|2169:FABP2|2168:FABP1|10554:AGPAT1|10555:AGPAT2|8611:PPAP2A|8613:PPAP2B|8612:PPAP2C|80168:MOGAT2|346606:MOGAT3|8694:DGAT1|84649:DGAT2|949:SCARB1|29881:NPC1L1|64240:ABCG5|64241:ABCG8|337:APOA4|338:APOB|4547:MTTP|335:APOA1|19:ABCA1|10999:SLC27A4|39:ACAT2	Familial amyloidosis|Hypoalphalipoproteinemia|CD36 deficiency	Ezetimibe (JAN/USAN/INN)	Fat is an important energy source from food. More than 95% of dietary fat is long-chain triacylglycerols (TAG), the remaining being phospholipids (4.5%) and sterols. In the small intestine lumen, dietary TAG is hydrolyzed to fatty acids (FA) and monoacylglycerols (MAG) by pancreatic lipase. These products are then emulsified with the help of phospholipids (PL) and bile acids (BA) present in bile to form micelles. Free FAs and MAGs are taken up by the enterocyte where they are rapidly resynthesized in endoplasmic reticulum (ER) to form TAG. PLs from the diet as well as bile - mainly LPA - too are absorbed by the enterocyte and are acylated to form phosphatidic acid (PA), which is also converted into TAG. Absorbed cholesterol (CL) is acylated to cholesterol esters (CE). Within the ER, TAG joins CE and apolipoprotein B (ApoB) to form chylomicrons that enter circulation through the lymph.
hsa05140	Leishmaniasis - Homo sapiens (human)	Human Diseases; Infectious Diseases	7097:TLR2|7099:TLR4|4615:MYD88|3654:IRAK1|51135:IRAK4|7189:TRAF6|6885:MAP3K7|10454:TAB1|23118:TAB2|4793:NFKBIB|4792:NFKBIA|4790:NFKB1|5970:RELA|3552:IL1A|3553:IL1B|3592:IL12A|3593:IL12B|7124:TNF|3565:IL4|4843:NOS2|3586:IL10|7040:TGFB1|7042:TGFB2|7043:TGFB3|718:C3|1378:CR1|3684:ITGAM|3689:ITGB2|100132941:uncharacterized|100291917:uncharacterized|2209:FCGR1A|9103:FCGR2C|2212:FCGR2A|2215:FCGR3B|2214:FCGR3A|3676:ITGA4|3688:ITGB1|5743:PTGS2|653361:NCF1|4688:NCF2|4689:NCF4|1535:CYBA|5594:MAPK1|5595:MAPK3|2002:ELK1|2353:FOS|3725:JUN|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|3458:IFNG|3459:IFNGR1|3460:IFNGR2|3716:JAK1|3717:JAK2|6772:STAT1|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|65108:MARCKSL1|5777:PTPN6|5579:PRKCB	Leishmaniasis		Leishmania is an intracellular protozoan parasite of macrophages that causes visceral, mucosal, and cutaneous diseases. The parasite is transmitted to humans by sandflies, where they survive and proliferate intracellularly by deactivating the macrophage. Successful infection of Leishmania is achieved by alteration of signaling events in the host cell, leading to enhanced production of the autoinhibitory molecules like TGF-beta and decreased induction of cytokines such as IL12 for protective immunity. Nitric oxide production is also inhibited. In addition, defective expression of major histocompatibility complex (MHC) genes silences subsequent T cell activation mediated by macrophages, resulting in abnormal immune responses.
hsa00300	Lysine biosynthesis - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	51166:AADAT|501:ALDH7A1	Hyperlysinemia		
hsa00591	Linoleic acid metabolism - Homo sapiens (human)	Metabolism; Lipid Metabolism	391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|151056:PLB1|246:ALOX15|1544:CYP1A2|1562:CYP2C18|1559:CYP2C9|1557:CYP2C19|1558:CYP2C8|1573:CYP2J2|1571:CYP2E1|1551:CYP3A7|1577:CYP3A5|64816:CYP3A43|1576:CYP3A4	Neurodegeneration with brain iron accumulation (NBIA)	Atreleuton (USAN/INN)|Benoxaprofen (USAN/INN)|Docebenone (USAN/INN)|Enazadrem phosphate (USAN)|Fenleuton (USAN/INN)|Lonapalene (USAN)	
hsa05030	Cocaine addiction - Homo sapiens (human)	Human Diseases; Substance Dependence	7054:TH|1644:DDC|6571:SLC18A2|6570:SLC18A1|4129:MAOB|4128:MAOA|6531:SLC6A3|1812:DRD1|2778:GNAS|2912:GRM2|2913:GRM3|2773:GNAI3|2770:GNAI1|2771:GNAI2|1813:DRD2|111:ADCY5|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|8787:RGS9|1385:CREB1|1386:ATF2|468:ATF4|10488:CREB3|64764:CREB3L2|84699:CREB3L3|148327:CREB3L4|90993:CREB3L1|9586:CREB5|1388:ATF6B|627:BDNF|3725:JUN|2354:FOSB|4790:NFKB1|5970:RELA|1020:CDK5|8851:CDK5R1|2903:GRIN2A|2904:GRIN2B|1742:DLG4|84152:PPP1R1B|2891:GRIA2|26086:GPSM1|5173:PDYN|116443:GRIN3A|116444:GRIN3B|2902:GRIN1|2905:GRIN2C|2906:GRIN2D			Drug addiction is a chronic, relapsing disorder in which compulsive drug-seeking and drug-taking behavior persists despite serious negative consequences.There is strong evidence that the dopaminergic system that projects from the ventral tegmental area (VTA) of the midbrain to the nucleus accumbens (NAc), and to other forebrain sites, is the major substrate of reward and reinforcement for both natural rewards and addictive drugs. Cocaine binds strongly to the dopamine-reuptake transporter, preventing the reuptake of dopamine into the nerve terminal. Because of this blocking effect, dopamine remains at high concentrations in the synapse and continues to affect adjacent neurons, producing the characteristic cocaine "high." Activated D1 receptor activates the PKA signaling pathway, and this pathway plays a critical role in mediating the behavioral responses to cocaine administration. Cocaine-induced neuroadaptations, including dopamine depletion, may underlie craving and hedonic dysregulation.
hsa00232	Caffeine metabolism - Homo sapiens (human)	Metabolism; Biosynthesis of Other Secondary Metabolites	1544:CYP1A2|9:NAT1|10:NAT2|1549:CYP2A7|1548:CYP2A6|1553:CYP2A13|7498:XDH		Febuxostat (JAN/USAN/INN)|Oxypurinol (USAN)|Allopurinol sodium	
hsa04114	Oocyte meiosis - Homo sapiens (human)	Cellular Processes; Cell Growth and Death	3630:INS|3479:IGF1|3480:IGF1R|5241:PGR|367:AR|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|6790:AURKA|64506:CPEB1|4342:MOS|5604:MAP2K1|5594:MAPK1|5595:MAPK3|6195:RPS6KA1|6196:RPS6KA2|6197:RPS6KA3|27330:RPS6KA6|9088:PKMYT1|7529:YWHAB|7532:YWHAG|7533:YWHAH|10971:YWHAQ|7534:YWHAZ|7531:YWHAE|387778:SPDYC|245711:SPDYA|983:CDK1|1017:CDK2|5501:PPP1CC|5499:PPP1CA|5500:PPP1CB|9748:SLK|5347:PLK1|995:CDC25C|9978:RBX1|8454:CUL1|6500:SKP1|23291:FBXW11|8945:BTRC|26271:FBXO5|64682:ANAPC1|29882:ANAPC2|996:CDC27|29945:ANAPC4|51433:ANAPC5|8881:CDC16|51434:ANAPC7|8697:CDC23|10393:ANAPC10|51529:ANAPC11|246184:CDC26|25847:ANAPC13|991:CDC20|286151:FBXO43|10744:PTTG2|9232:PTTG1|9700:ESPL1|9985:REC8|10734:STAG3|8243:SMC1A|27127:SMC1B|9126:SMC3|699:BUB1|4085:MAD2L1|10459:MAD2L2|9134:CCNE2|898:CCNE1|151648:SGOL1|5525:PPP2R5A|5528:PPP2R5D|5526:PPP2R5B|5527:PPP2R5C|5529:PPP2R5E|5518:PPP2R1A|5519:PPP2R1B|5516:PPP2CB|5515:PPP2CA|89869:PLCZ1|3708:ITPR1|3709:ITPR2|3710:ITPR3|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|6300:MAPK12|891:CCNB1|9133:CCNB2	Coffin-Lowry syndrome (CLS)|46,XY disorders of sex development (Disorders in androgen synthesis or action)|Cornelia de Lange syndrome (CdLS)	Progesterone (JP16/USP/INN)|Norethisterone (JP16)|Danazol (JP16/USP/INN)|Mifepristone (USAN/INN)|Hydroxyprogesterone caproate (JAN/USP/INN)|Levonorgestrel (JAN/USP/INN)|Medroxyprogesterone acetate (JAN/USP)|Megestrol acetate (USAN)|Norethisterone acetate (JAN)|Norgestrel (JP16/USP/INN)|Gestonorone caproate (JAN/USAN)|Dydrogesterone (JP16/USP/INN)|Ethynodiol diacetate (JAN/USP)|Chlormadinone acetate (JP16/USAN)|Allylestrenol (JAN/INN)|Lynestrenol (JAN/USAN)|Desogestrel (USAN/INN)|Asoprisnil (USAN/INN)|Mecasermin (genetical recombination) (JAN)|Dienogest (JAN/USAN/INN)|Etonogestrel (USAN/INN)|Gestodene (USAN/INN)|Mecasermin rinfabate (USAN/INN)|Medrogestone (USAN/INN)|Mesterolone (USAN/INN)|Methynodiol diacetate (USAN)|Mibolerone (USP/INN)|Norgestimate (USP/INN)|Quingestanol acetate (USAN)|Norgestrienone (INN)|Nomegestrol (USAN/INN)|Demegestone (INN)|Chlormadinone (INN)|Etynodiol (INN)|Hydroxyprogesterone (INN)|Hydroxyprogesterone 17alfa-acetate|Medroxyprogesterone (INN)|Megestrol (INN)|Nomegestrol acetate (USAN)|Norethisterone enantate|Promegestone (INN)	During meiosis, a single round of DNA replication is followed by two rounds of chromosome segregation, called meiosis I and meiosis II. At meiosis I, homologous chromosomes recombine and then segregate to opposite poles, while the sister chromatids segregate from each other at meoisis II. In vertebrates, immature oocytes are arrested at the PI (prophase of meiosis I). The resumption of meiosis is stimulated by progesterone, which carries the oocyte through two consecutive M-phases (MI and MII) to a second arrest at MII. The key activity driving meiotic progression is the MPF (maturation-promoting factor), a heterodimer of CDC2 (cell division cycle 2 kinase) and cyclin B. In PI-arrested oocytes, MPF is initially inactive and is activated by the dual-specificity CDC25C phosphatase as the result of new synthesis of Mos induced by progesterone. MPF activation mediates the transition from the PI arrest to MI. The subsequent decrease in MPF levels, required to exit from MI into interkinesis, is induced by a negative feedback loop, where CDC2 brings about the activation of the APC (anaphase-promoting complex), which mediates destruction of cyclin B. Re-activation of MPF for MII requires re-accumulation of high levels of cyclin B as well as the inactivation of the APC by newly synthesized Emi2 and other components of the CSF (cytostatic factor), such as cyclin E or high levels of Mos. CSF antagonizes the ubiquitin ligase activity of the APC, preventing cyclin B destruction and meiotic exit until fertilization occurs. Fertilization triggers a transient increase in cytosolic free Ca2+, which leads to CSF inactivation and cyclin B destruction through the APC. Then eggs are released from MII into the first embryonic cell cycle.
hsa05134	Legionellosis - Homo sapiens (human)	Human Diseases; Infectious Diseases	3329:HSPD1|718:C3|1378:CR1|3684:ITGAM|3689:ITGB2|375:ARF1|5861:RAB1A|81876:RAB1B|9554:SEC22B|56681:SAR1A|51128:SAR1B|7415:VCP|317:APAF1|54205:CYCS|842:CASP9|836:CASP3|841:CASP8|664:BNIP3|23786:BCL2L13|4791:NFKB2|4792:NFKBIA|4790:NFKB1|5970:RELA|10767:HBS1L|1917:EEF1A2|1915:EEF1A1|3297:HSF1|3306:HSPA2|3310:HSPA6|3304:HSPA1B|3305:HSPA1L|3312:HSPA8|3303:HSPA1A|1937:EEF1G|4671:NAIP|840:CASP7|58484:NLRC4|29108:PYCARD|834:CASP1|3606:IL18|3553:IL1B|7100:TLR5|7097:TLR2|929:CD14|7099:TLR4|4615:MYD88|7124:TNF|3569:IL6|3592:IL12A|3593:IL12B|3576:IL8|2921:CXCL3|2920:CXCL2|2919:CXCL1|1195:CLK1	Legionellosis		Legionellosis is a potentially fatal infectious disease caused by the bacterium Legionella pneumophila and other legionella species. Two distinct clinical and epidemiological syndromes are associated with Legionella species: Legionnaires' disease is the more severe form of the infection, which may involve pneumonia, and Pontiac fever is a milder respiratory illness.|The pathogenesis of L. pneumophila is derived from its growth within lung macrophages. One of the L. pneumophila's type IV secretion systems, the Dot/Icm secretion system, is of critical importance for its ability to replicate and to cause disease. The Dot/Icm substrates modulate multiple host cell processes and in particular, redirect trafficking of the L. pneumophila phagosome and mediate its conversion into an ER-derived organelle competent for intracellular bacterial replication. L. pneumophila also manipulates host cell death and survival pathways in a way that allows continued intracellular replication.
hsa05310	Asthma - Homo sapiens (human)	Human Diseases; Immune Diseases	3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|3565:IL4|959:CD40LG|958:CD40|100132941:uncharacterized|100291917:uncharacterized|2205:FCER1A|2206:MS4A2|2207:FCER1G|3578:IL9|3586:IL10|3596:IL13|3567:IL5|7124:TNF|3562:IL3|5553:PRG2|6037:RNASE3|8288:EPX|6356:CCL11	Asthma|Eosinophil peroxidase deficiency	Golimumab (genetical recombination) (JAN)|Omalizumab (genetical recombination) (JAN)	Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation.
hsa05322	Systemic lupus erythematosus - Homo sapiens (human)	Human Diseases; Immune Diseases	712:C1QA|713:C1QB|714:C1QC|717:C2|720:C4A|721:C4B|55506:H2AFY2|3014:H2AFX|8969:HIST1H2AG|8335:HIST1H2AB|3013:HIST1H2AD|3012:HIST1H2AE|9555:H2AFY|8331:HIST1H2AJ|3015:H2AFZ|8336:HIST1H2AM|8337:HIST2H2AA3|8330:HIST1H2AK|8332:HIST1H2AL|8329:HIST1H2AI|8334:HIST1H2AC|55766:H2AFJ|94239:H2AFV|85235:HIST1H2AH|92815:HIST3H2A|83740:H2AFB3|8338:HIST2H2AC|474382:H2AFB1|474381:H2AFB2|723790:HIST2H2AA4|317772:HIST2H2AB|221613:HIST1H2AA|286436:H2BFM|3017:HIST1H2BD|8348:HIST1H2BO|8344:HIST1H2BE|8345:HIST1H2BH|8346:HIST1H2BI|8347:HIST1H2BC|3018:HIST1H2BB|8970:HIST1H2BJ|8339:HIST1H2BG|8340:HIST1H2BL|8341:HIST1H2BN|8342:HIST1H2BM|8343:HIST1H2BF|128312:HIST3H2BB|158983:H2BFWT|85236:HIST1H2BK|8349:HIST2H2BE|440689:HIST2H2BF|255626:HIST1H2BA|653604:HIST2H3D|8350:HIST1H3A|8352:HIST1H3C|8358:HIST1H3B|8353:HIST1H3E|8356:HIST1H3J|8355:HIST1H3G|8354:HIST1H3I|3021:H3F3B|8357:HIST1H3H|8968:HIST1H3F|8351:HIST1H3D|3020:H3F3A|8290:HIST3H3|126961:HIST2H3C|333932:HIST2H3A|440093:H3F3C|8359:HIST1H4A|8364:HIST1H4C|8360:HIST1H4D|8365:HIST1H4H|8362:HIST1H4K|8366:HIST1H4B|8367:HIST1H4E|8361:HIST1H4F|8368:HIST1H4L|8369:HIST1H4G|8363:HIST1H4J|8370:HIST2H4A|8294:HIST1H4I|121504:HIST4H4|554313:HIST2H4B|6628:SNRPB|6632:SNRPD1|6634:SNRPD3|2903:GRIN2A|2904:GRIN2B|6737:TRIM21|6738:TROVE2|6741:SSB|81:ACTN4|88:ACTN2|87:ACTN1|89:ACTN3|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|941:CD80|942:CD86|940:CD28|959:CD40LG|958:CD40|7124:TNF|3458:IFNG|3586:IL10|100132941:uncharacterized|100291917:uncharacterized|715:C1R|716:C1S|718:C3|727:C5|729:C6|730:C7|731:C8A|732:C8B|733:C8G|735:C9|1511:CTSG|1991:ELANE|2209:FCGR1A|9103:FCGR2C|2212:FCGR2A|2213:FCGR2B|2215:FCGR3B|2214:FCGR3A	Systemic lupus erythematosus		Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterised by the production of IgG autoantibodies that are specific for self-antigens, such as DNA, nuclear proteins and certain cytoplasmic components, in association with a diverse array of clinical manifestations. The primary pathological findings in patients with SLE are those of inflammation, vasculitis, immune complex deposition, and vasculopathy. Immune complexes comprising autoantibody and self-antigen is deposited particulary in the renal glomeruli and mediate a systemic inflammatory response by activating complement or via Fc{gamma}R-mediated neutrophil and macrophage activation. Activation of complement (C5) leads to injury both through formation of the membrane attack complex (C5b-9) or by generation of the anaphylatoxin and cell activator C5a. Neutrophils and macrophages cause tissue injury by the release of oxidants and proteases.
hsa05215	Prostate cancer - Homo sapiens (human)	Human Diseases; Cancers	1027:CDKN1B|1017:CDK2|9134:CCNE2|898:CCNE1|5925:RB1|1871:E2F3|1869:E2F1|1870:E2F2|3630:INS|5154:PDGFA|5155:PDGFB|56034:PDGFC|80310:PDGFD|1950:EGF|7039:TGFA|3479:IGF1|3645:INSRR|5156:PDGFRA|5159:PDGFRB|2260:FGFR1|2263:FGFR2|1956:EGFR|2064:ERBB2|3480:IGF1R|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5728:PTEN|5170:PDPK1|4824:NKX3-1|207:AKT1|208:AKT2|10000:AKT3|842:CASP9|572:BAD|2308:FOXO1|1026:CDKN1A|4193:MDM2|7157:TP53|2932:GSK3B|1385:CREB1|468:ATF4|10488:CREB3|64764:CREB3L2|84699:CREB3L3|148327:CREB3L4|90993:CREB3L1|9586:CREB5|1499:CTNNB1|1387:CREBBP|2033:EP300|6932:TCF7|83439:TCF7L1|6934:TCF7L2|51176:LEF1|595:CCND1|1147:CHUK|3551:IKBKB|8517:IKBKG|4792:NFKBIA|4790:NFKB1|5970:RELA|596:BCL2|2475:MTOR|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|6716:SRD5A2|367:AR|3320:HSP90AA1|3326:HSP90AB1|7184:HSP90B1|354:KLK3|2950:GSTP1	Prostate cancer	Testosterone (JAN/USP)|Finasteride (JAN/USP/INN)|Flutamide (JP16/USP/INN)|Bicalutamide (JAN/USP/INN)|Nilutamide (USAN/INN)|Dutasteride (JAN/USAN/INN)|Idronoxil (USAN/INN)	Prostate cancer constitutes a major health problem in Western countries. It is the most frequently diagnosed cancer among men and the second leading cause of male cancer deaths. The identification of key molecular alterations in prostate-cancer cells implicates carcinogen defenses (GSTP1), growth-factor-signaling pathways (NKX3.1, PTEN, and p27), and androgens (AR) as critical determinants of the phenotype of prostate-cancer cells. Glutathione S-transferases (GSTP1) are detoxifying enzymes. Cells of prostatic intraepithelial neoplasia, devoid of GSTP1, undergo genomic damage mediated by carcinogens. NKX3.1, PTEN, and p27 regulate the growth and survival of prostate cells in the normal prostate. Inadequate levels of PTEN and NKX3.1 lead to a reduction in p27 levels and to increased proliferation and decreased apoptosis. Androgen receptor (AR) is a transcription factor that is normally activated by its androgen ligand. During androgen withdrawal therapy, the AR signal transduction pathway also could be activated by amplification of the AR gene, by AR gene mutations, or by altered activity of AR coactivators. Through these mechanisms, tumor cells lead to the emergence of androgen-independent prostate cancer.
hsa05133	Pertussis - Homo sapiens (human)	Human Diseases; Infectious Diseases	3678:ITGA5|3688:ITGB1|3684:ITGAM|3689:ITGB2|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|387:RHOA|1072:CFL1|1073:CFL2|836:CASP3|840:CASP7|834:CASP1|29108:PYCARD|114548:NLRP3|3553:IL1B|712:C1QA|713:C1QB|714:C1QC|715:C1R|716:C1S|717:C2|720:C4A|721:C4B|718:C3|727:C5|710:SERPING1|722:C4BPA|725:C4BPB|23643:LY96|7099:TLR4|929:CD14|114609:TIRAP|4615:MYD88|51135:IRAK4|3654:IRAK1|7189:TRAF6|4790:NFKB1|5970:RELA|353376:TICAM2|148022:TICAM1|3661:IRF3|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|5602:MAPK10|5601:MAPK9|5599:MAPK8|5594:MAPK1|5595:MAPK3|2353:FOS|3725:JUN|3569:IL6|3592:IL12A|3593:IL12B|51561:IL23A|7124:TNF|3586:IL10|3659:IRF1|3394:IRF8|653509:SFTPA1|2773:GNAI3|2770:GNAI1|2771:GNAI2|3576:IL8|6374:CXCL5|6372:CXCL6|10392:NOD1|3552:IL1A|4843:NOS2	Pertussis		Pertussis, also known as whooping cough, is an acute respiratory infectious disease caused by a bacteria called Bordetella Pertussis. The characteristic symptoms are paroxysmal cough, inspiratory wheezing and post-tussive vomiting.|Following the inhalation of respiratory secretions from an infected individual, bacteria enter the upper respiratory tract and adhere to epithelial cells. Several adhesion factors have been implicated: the filamentous hemagglutinin (FHA), fimbriae, and pertactin (Prn).|Pertussis toxin (Ptx) and adenylate cyclase toxin (ACT) have been identified so far as major protein toxins of B. pertussis. PTX is a hexameric AB5-type exotoxin. Catalytic A subunit catalyzes the ADP-ribosylation of the Gi subunits of the heterotrimeric G protein, then inhibits multiple downstream pathways. ACT is able to penetrate the cytoplasmic membrane of host cells and becomes activated through the cleavage and the binding of calmodulin (CaM). Activated ACT converts ATP to cyclic AMP and subverts cellular signaling pathways.
hsa04510	Focal adhesion - Homo sapiens (human)	Cellular Processes; Cell Communication	1280:COL2A1|1302:COL11A2|1301:COL11A1|1277:COL1A1|1289:COL5A1|50509:COL5A3|1281:COL3A1|1290:COL5A2|1278:COL1A2|1284:COL4A2|1286:COL4A4|1288:COL4A6|1287:COL4A5|1282:COL4A1|1292:COL6A2|1291:COL6A1|1293:COL6A3|131873:COL6A6|284217:LAMA1|3908:LAMA2|3911:LAMA5|3909:LAMA3|3910:LAMA4|3912:LAMB1|3913:LAMB2|3914:LAMB3|22798:LAMB4|3915:LAMC1|3918:LAMC2|10319:LAMC3|1101:CHAD|5649:RELN|1311:COMP|7059:THBS3|7058:THBS2|7060:THBS4|7057:THBS1|2335:FN1|6696:SPP1|7448:VTN|63923:TNN|7143:TNR|7148:TNXB|3371:TNC|7450:VWF|3381:IBSP|3672:ITGA1|3673:ITGA2|3674:ITGA2B|3675:ITGA3|3676:ITGA4|3678:ITGA5|3655:ITGA6|3679:ITGA7|8516:ITGA8|3680:ITGA9|8515:ITGA10|22801:ITGA11|3685:ITGAV|3688:ITGB1|3690:ITGB3|3691:ITGB4|3693:ITGB5|3694:ITGB6|3695:ITGB7|3696:ITGB8|5154:PDGFA|5155:PDGFB|56034:PDGFC|80310:PDGFD|1950:EGF|3479:IGF1|7423:VEGFB|5228:PGF|7422:VEGFA|7424:VEGFC|2277:FIGF|3082:HGF|5156:PDGFRA|5159:PDGFRB|3480:IGF1R|3791:KDR|1956:EGFR|2321:FLT1|2324:FLT4|4233:MET|2064:ERBB2|6714:SRC|2909:ARHGAP35|394:ARHGAP5|387:RHOA|1729:DIAPH1|6093:ROCK1|9475:ROCK2|4633:MYL2|4636:MYL5|58498:MYL7|10398:MYL9|93408:MYL10|10627:MYL12A|103910:MYL12B|29895:MYLPF|5501:PPP1CC|5499:PPP1CA|5500:PPP1CB|4659:PPP1R12A|4638:MYLK|85366:MYLK2|91807:MYLK3|60:ACTB|71:ACTG1|5923:RASGRF1|824:CAPN2|81:ACTN4|88:ACTN2|87:ACTN1|89:ACTN3|7094:TLN1|83660:TLN2|2317:FLNB|2318:FLNC|2316:FLNA|5829:PXN|3611:ILK|7791:ZYX|7408:VASP|7414:VCL|55742:PARVA|64098:PARVG|29780:PARVB|5170:PDPK1|207:AKT1|208:AKT2|10000:AKT3|2932:GSK3B|1499:CTNNB1|5579:PRKCB|5578:PRKCA|5582:PRKCG|5747:PTK2|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5728:PTEN|10451:VAV3|7409:VAV1|7410:VAV2|5879:RAC1|5880:RAC2|5881:RAC3|5058:PAK1|5062:PAK2|5063:PAK3|10298:PAK4|56924:PAK6|57144:PAK7|998:CDC42|9564:BCAR1|1399:CRKL|1398:CRK|1793:DOCK1|2889:RAPGEF1|5906:RAP1A|5908:RAP1B|5602:MAPK10|5601:MAPK9|5599:MAPK8|3725:JUN|673:BRAF|857:CAV1|858:CAV2|859:CAV3|2534:FYN|25759:SHC2|6464:SHC1|53358:SHC3|399694:SHC4|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|5894:RAF1|5604:MAP2K1|5594:MAPK1|5595:MAPK3|2002:ELK1|595:CCND1|894:CCND2|896:CCND3|572:BAD|596:BCL2|23396:PIP5K1C|329:BIRC2|330:BIRC3|331:XIAP	Glanzmann thrombasthenia|PTEN hamartoma tumor syndrome (PHTS)|Caveolinopathies|Pierson syndrome|Syndromic X-linked mental retardation with epilepsy or seizures|Hereditary angiopathy with nephropathy, aneurysms, and muscle cramps (HANAC)|Alport syndrome|Benign familial hematuria|Epidermolysis bullosa, hemidesmosomal|Epidermolysis bullosa, junctional|Congenital muscular dystrophies (CMD/MDC)|Limb-girdle muscular dystrophy (LGMD)|Myofibrillar myopathies (MFM)|Nephrotic syndrome and focal segmental glomerulosclerosis|Familial thoracic aortic aneurysm and dissection (TAAD)|Ehlers-Danlos syndrome (EDS)|Vitreoretinal degeneration|Laryngoonychocutaneous syndrome|Porencephaly|Lethal congenital contractural syndrome (LCCS)|Brain small vessel disease with Axenfeld-Rieger anomaly|FG syndrome (FGS)|Pilomatricoma|VACTERL/VATER association|Hypomagnesemia	Becaplermin (USAN/INN)|Mecasermin (genetical recombination) (JAN)|Cilengitide (USAN/INN)|Mecasermin rinfabate (USAN/INN)|Semaxanib (USAN/INN)|Tivozanib (USAN/INN)|Lenvatinib (USAN/INN)|Lenvatinib mesylate (USAN)|Valategrast hydrochloride (USAN)	Cell-matrix adhesions play essential roles in important biological processes including cell motility, cell proliferation, cell differentiation, regulation of gene expression and cell survival. At the cell-extracellular matrix contact points, specialized structures are formed and termed focal adhesions, where bundles of actin filaments are anchored to transmembrane receptors of the integrin family through a multi-molecular complex of junctional plaque proteins. Some of the constituents of focal adhesions participate in the structural link between membrane receptors and the actin cytoskeleton, while others are signalling molecules, including different protein kinases and phosphatases, their substrates, and various adapter proteins. Integrin signaling is dependent upon the non-receptor tyrosine kinase activities of the FAK and src proteins as well as the adaptor protein functions of FAK, src and Shc to initiate downstream signaling events. These signalling events culminate in reorganization of the actin cytoskeleton; a prerequisite for changes in cell shape and motility, and gene expression. Similar morphological alterations and modulation of gene expression are initiated by the binding of growth factors to their respective receptors, emphasizing the considerable crosstalk between adhesion- and growth factor-mediated signalling.
hsa00982	Drug metabolism - cytochrome P450 - Homo sapiens (human)	Metabolism; Xenobiotics Biodegradation and Metabolism	1565:CYP2D6|1551:CYP3A7|1577:CYP3A5|64816:CYP3A43|1576:CYP3A4|2327:FMO2|2330:FMO5|2326:FMO1|2329:FMO4|2328:FMO3|1562:CYP2C18|1559:CYP2C9|1557:CYP2C19|1558:CYP2C8|1555:CYP2B6|4257:MGST1|4258:MGST2|2940:GSTA3|2939:GSTA2|2946:GSTM2|2941:GSTA4|2948:GSTM4|2953:GSTT2|2949:GSTM5|2947:GSTM3|9446:GSTO1|4259:MGST3|119391:GSTO2|2938:GSTA1|2952:GSTT1|2944:GSTM1|2950:GSTP1|221357:GSTA5|373156:GSTK1|126:ADH1C|131:ADH7|124:ADH1A|125:ADH1B|127:ADH4|128:ADH5|130:ADH6|222:ALDH3B2|220:ALDH1A3|221:ALDH3B1|218:ALDH3A1|4129:MAOB|4128:MAOA|316:AOX1|7363:UGT2B4|574537:UGT2A2|7367:UGT2B17|7365:UGT2B10|7364:UGT2B7|7366:UGT2B15|54577:UGT1A7|10720:UGT2B11|54490:UGT2B28|54579:UGT1A5|54659:UGT1A3|54657:UGT1A4|54578:UGT1A6|54576:UGT1A8|54600:UGT1A9|10941:UGT2A1|54575:UGT1A10|79799:UGT2A3|54658:UGT1A1|1544:CYP1A2|1571:CYP2E1|1549:CYP2A7|1548:CYP2A6|1553:CYP2A13	Poor drug metabolism (PM)|Coumarin resistance	Isoniazid (JP16/USP/INN)|Phenelzine sulfate (USP)|Fomepizole (USAN/INN)|Selegiline hydrochloride (JAN/USP)|Tranylcypromine sulfate (USP XXI)|Lazabemide hydrochloride (JAN/USAN)|Amezinium metilsulfate (JAN)|Isoniazid calcium pyruvinate (JAN)|Safrazine hydrochloride (JAN)|Isoniazid sodium methanesulfonate hydrate (JAN)|Toloxatone (INN)|Brofaromine (INN)|Moclobemide (USAN/INN)|Rasagiline mesylate (USAN)|Befloxatone (INN)|Pargyline hydrochloride (USAN)|Iproniazid (INN)|Isocarboxazid (INN)|Cimoxatone (INN)|Ladostigil tartrate (USAN)|Clorgiline (INN)|Caroxazone (USAN/INN)|Selegiline (USAN/INN)|Mofegiline hydrochloride (USAN)|Lazabemide (USAN/INN)|Milacemide hydrochloride (USAN)|Nialamide (INN)|Iproclozide (INN)|Iproniazid phosphate|Phenelzine (BAN)|Pargyline (INN)|Rasagiline (USAN/INN)|Tranylcypromine (INN)	
hsa04742	Taste transduction - Homo sapiens (human)	Organismal Systems; Sensory System	6337:SCNN1A|6338:SCNN1B|6340:SCNN1G|40:ASIC2|773:CACNA1A|774:CACNA1B|2914:GRM4|80835:TAS1R1|83756:TAS1R3|2782:GNB1|2784:GNB3|2785:GNG3|51764:GNG13|259285:TAS2R39|353164:TAS2R42|5726:TAS2R38|50832:TAS2R4|54429:TAS2R5|50831:TAS2R3|50836:TAS2R8|50840:TAS2R14|50839:TAS2R10|50835:TAS2R9|50837:TAS2R7|50833:TAS2R16|50838:TAS2R13|50834:TAS2R1|259286:TAS2R40|259294:TAS2R19|259295:TAS2R20|259296:TAS2R50|259291:TAS2R45|259287:TAS2R41|259292:TAS2R46|259289:TAS2R43|338398:TAS2R60|259290:TAS2R31|3710:ITPR3|29850:TRPM5|80834:TAS1R2|2778:GNAS|196883:ADCY4|112:ADCY6|114:ADCY8|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|3745:KCNB1|346562:GNAT3|5136:PDE1A|5330:PLCB2		Triamterene (JP16/USP/INN)	All taste pathways are proposed to converge on common elements that mediate a rise in intracellular Ca2+ followed by neurotransmitter release. Na+ salt depolarizes taste cells by passive influx of Na+ through the amiloride-sensitive Na+ channel (ENaC). Acids depolarize taste cells by a variety of mechanisms, including influx of protons (H+) through ENaC and a proton-gated cation channel (MDEG). Two putative umami receptors have been identified: a truncated variant of the metabotropic glutamate receptor mGluR4 and the heterodimer, T1R1 + T1R3. Umami receptors are coupled to a signaling pathway involving activation of PLCbeta2, production of IP3 and diacylglycerol, release of Ca2+ from intracellular stores and activation of a transient receptor potential channel, TRPM5. Bitter compounds, such as denatonium and PROP, activate particular T2R/TRB isoforms, which activate gustducin heterotrimers. Activated alpha-gustducin stimulates PDE to hydrolyze cAMP, whereas betagamma subunits activate PLCbeta2 to generate IP3, which leads to release of Ca2+ from internal stores. Artificial sweeteners activate GPCRs (T1R heterodimers) apparently linked via PLC to IP3 production and release of Ca2+ from intracellular stores. Sugars apparently activate GPCRs linked via AC to cAMP production which, in turn, may inhibit basolateral K+ channels through phosphorylation by cAMP-activated protein kinase A (PKA).
hsa00524	Butirosin and neomycin biosynthesis - Homo sapiens (human)	Metabolism; Biosynthesis of Other Secondary Metabolites	3101:HK3|3099:HK2|3098:HK1|80201:HKDC1|2645:GCK			
hsa00051	Fructose and mannose metabolism - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	4351:MPI|5373:PMM2|5372:PMM1|29925:GMPPB|29926:GMPPA|2762:GMDS|7264:TSTA3|8790:FPGT|197258:FUK|3101:HK3|3099:HK2|3098:HK1|80201:HKDC1|5214:PFKP|5211:PFKL|5213:PFKM|8789:FBP2|2203:FBP1|5210:PFKFB4|5208:PFKFB2|5209:PFKFB3|5207:PFKFB1|57103:C12orf5|9107:MTMR6|8776:MTMR1|9108:MTMR7|29085:PHPT1|8898:MTMR2|57016:AKR1B10|3795:KHK|6652:SORD|231:AKR1B1|229:ALDOB|230:ALDOC|226:ALDOA|7167:TPI1	Congenital disorders of glycosylation (CDG) type I	Epalrestat (JAN/INN)|Fidarestat (JAN/INN)|Tolrestat (USAN/INN)|Zopolrestat (USAN/INN)|Alrestatin sodium (USAN)|Lidorestat (USAN)|Minalrestat (USAN/INN)|Ponalrestat (USAN/INN)|Zenarestat (USAN/INN)|Sorbinil (USAN/INN)	
hsa04972	Pancreatic secretion - Homo sapiens (human)	Organismal Systems; Digestive System	1131:CHRM3|886:CCKAR|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|5579:PRKCB|5578:PRKCA|5582:PRKCG|9545:RAB3D|4218:RAB8A|8766:RAB11A|5874:RAB27B|5906:RAP1A|5908:RAP1B|387:RHOA|5879:RAC1|5646:PRSS3|5645:PRSS2|5644:PRSS1|1506:CTRL|51032:CELA2B|63036:CELA2A|10136:CELA3A|23436:CELA3B|1357:CPA1|1358:CPA2|1359:CPA3|1360:CPB1|1361:CPB2|5406:PNLIP|5407:PNLIPRP1|5408:PNLIPRP2|1056:CEL|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|3708:ITPR1|3709:ITPR2|3710:ITPR3|6262:RYR2|683:BST1|952:CD38|219931:TPCN2|488:ATP2A2|489:ATP2A3|487:ATP2A1|1179:CLCA1|9635:CLCA2|22802:CLCA4|7220:TRPC1|6558:SLC12A2|476:ATP1A1|480:ATP1A4|478:ATP1A3|477:ATP1A2|481:ATP1B1|482:ATP1B2|483:ATP1B3|23439:ATP1B4|486:FXYD2|3784:KCNQ1|3778:KCNMA1|491:ATP2B2|490:ATP2B1|493:ATP2B4|492:ATP2B3|6548:SLC9A1|6522:SLC4A2|6344:SCTR|2778:GNAS|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|1080:CFTR|1811:SLC26A3|8671:SLC4A4|1504:CTRB1|279:AMY2A|280:AMY2B|760:CA2	Hereditary pancreatitis	Atropine (USP)|Acarbose (JAN/USAN/INN)|Pilocarpine (JAN/USP)|Oxybutynin hydrochloride (JAN)|Oxyphencyclimine hydrochloride (JAN)|Tolterodine tartrate (JAN/USAN)|Solifenacin succinate (JAN/USAN/INN)|Azosemide (JAN/USAN/INN)|Pipethanate hydrochloride (JAN)|Piretanide (JAN/USAN/INN)|Darifenacin hydrobromide (JAN/USAN)|Proglumide (JP16/USAN/INN)|Panazepide (JAN)|Tiquizium bromide (JAN/INN)|Tiotropium bromide hydrate (JAN)|N-Methylscopolamine methylsulfate (JAN)|Secretin (JAN/USAN/INN)|Atropine sulfate (JP16/USP)|Homatropine methylbromide (USP)|Pilocarpine hydrochloride (JP16/USP)|Devazepide (USAN/INN)|Tarazepide (INN)|Alvameline maleate (USAN)|Darifenacin (USAN/INN)|Dexetimide (USAN/INN)|Esoxybutynin chloride (USAN)|Methacholine chloride (USAN/INN)|Pilocarpine nitrate (USP)|Imidafenacin (JAN/INN)|Cimetropium bromide (INN)|Cevimeline (INN)|Oxyphencyclimine (INN)|Pilocarpine borate|Piperidolate (INN)|Solifenacin (INN)|Trimebutine (INN)|Carpronium chloride hydrate (JAN)	The pancreas performs both exocrine and endocrine functions.  The exocrine pancreas consists of two parts, the acinar and duct cells. The primary functions of pancreatic acinar cells are to synthesize and secrete digestive enzymes. Stimulation of the cell by secretagogues such as acetylcholine (ACh) and cholecystokinin (CCK) causes the generation of an intracellular Ca2+ signal. This signal, in turn, triggers the fusion of the zymogen granules with the apical plasma membrane, leading to the polarised secretion of the enzymes. The major task of pancreatic duct cells is the secretion of fluid and bicarbonate ions (HCO3-), which neutralize the acidity of gastric contents that enter the duodenum. An increase in intracellular cAMP by secretin is one of the major signals of pancreatic HCO3- secretion. Activation of the CFTR Cl- channel and the CFTR-dependent Cl-/HCO3- exchange activities is responsible for cAMP-induced HCO3- secretion.
hsa01100	Metabolic pathways - Homo sapiens (human)			Desmosterolosis|Delayed sleep phase syndrome|Lamellar ichthyosis (LI) and Non-bullous congenital ichthyosiform erythroderma (NBCIE)|Urofacial syndrome|SEMD, Pakistani type|Multiple cutaneous and uterine leiomyomata|Calcification of joints and arteries|Exocrine pancreatic insufficiency, dyserythropoietic anemia, and calvarial hyperostosis|Arts syndrome|Generalized arterial calcification of infancy	Trapidil (JP16/INN)|Naproxen etemesil (USAN)	
hsa00450	Selenocompound metabolism - Homo sapiens (human)	Metabolism; Metabolism of Other Amino Acids	4548:MTR|1491:CTH|51540:SCLY|883:CCBL1|56267:CCBL2|114112:TXNRD3|10587:TXNRD2|7296:TXNRD1|11185:INMT|9060:PAPSS2|9061:PAPSS1|22929:SEPHS1|22928:SEPHS2|118672:PSTK|51091:SEPSECS|92935:MARS2|4141:MARS	Homocystinuria|Hypermethioninemia|SEMD, Pakistani type		
hsa00130	Ubiquinone and other terpenoid-quinone biosynthesis - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	6898:TAT|27235:COQ2|51805:COQ3|51004:COQ6|84274:COQ5|10229:COQ7|3242:HPD	Coenzyme Q10 deficiency	Nitisinone (JAN/USAN/INN)	Ubiquinone (UQ), also called coenzyme Q, and plastoquinone (PQ) are electron carriers in oxidative phosphorylation and photosynthesis, respectively. The quinoid nucleus of ubiquinone is derived from the shikimate pathway; 4-hydroxybenzoate is directly formed from chorismate in bacteria, while it can be formed from either chorismate or tyrosine in yeast. The following biosynthesis of terpenoid moiety involves reactions of prenylation, decarboxylation, and three hydroxylations alternating with three methylations. The order of these reactions are somewhat different between bacteria and yeast. Phylloquinone (vitamin K1), menaquinone (vitamin K2), and tocopherol (vitamin E) are fat-soluble vitamins. Phylloquinone is a compound present in all photosynthetic plants serving as a cofactor for photosystem I-mediated electron transport. Menaquinone is an obligatory component of the electron-transfer pathway in bacteria.
hsa03015	mRNA surveillance pathway - Homo sapiens (human)	Genetic Information Processing; Translation	4686:NCBP1|22916:NCBP2|65110:UPF3A|65109:UPF3B|9939:RBM8A|4116:MAGOH|55110:MAGOHB|22794:CASC3|9775:EIF4A3|10284:SAP18|5411:PNN|22985:ACIN1|10921:RNPS1|10189:ALYREF|55998:NXF5|56000:NXF3|56001:NXF2|10482:NXF1|728343:NXF2B|55916:NXT2|29107:NXT1|7919:DDX39B|84305:WIBG|10250:SRRM1|8732:RNGTT|8731:RNMT|390748:PABPN1L|8106:PABPN1|11051:NUDT21|11052:CPSF6|79869:CPSF7|56903:PAPOLB|10914:PAPOLA|64895:PAPOLG|10978:CLP1|51585:PCF11|29894:CPSF1|53981:CPSF2|51692:CPSF3|10898:CPSF4|81608:FIP1L1|55339:WDR33|80335:WDR82|5501:PPP1CC|5499:PPP1CA|5500:PPP1CB|29101:SSU72|1477:CSTF1|1478:CSTF2|23283:CSTF2T|1479:CSTF3|8189:SYMPK|4440:MSI1|124540:MSI2|26528:DAZAP1|340529:PABPC1L2A|645974:PABPC1L2B|5042:PABPC3|8761:PABPC4|26986:PABPC1|132430:PABPC4L|140886:PABPC5|80336:PABPC1L|2107:ETF1|2935:GSPT1|23708:GSPT2|5976:UPF1|26019:UPF2|23049:SMG1|9887:SMG7|23381:SMG5|23293:SMG6|5516:PPP2CB|5515:PPP2CA|5518:PPP2R1A|5519:PPP2R1B|55844:PPP2R2D|5520:PPP2R2A|5522:PPP2R2C|5521:PPP2R2B|5523:PPP2R3A|28227:PPP2R3B|55012:PPP2R3C|5525:PPP2R5A|5528:PPP2R5D|5526:PPP2R5B|5527:PPP2R5C|5529:PPP2R5E|10767:HBS1L|53918:PELO	Syndromic X-linked mental retardation|Oculopharyngeal muscular dystrophy (OPMD)		The mRNA surveillance pathway is a quality control mechanism that detects and degrades abnormal mRNAs. These  pathways include nonsense-mediated mRNA decay (NMD), nonstop mRNA decay (NSD), and no-go decay (NGD). NMD is a mechanism that eliminates mRNAs containing premature translation-termination codons (PTCs). In vertebrates, PTCs trigger efficient NMD when located upstream of an exon junction complex (EJC). Upf3, together with Upf1 and Upf2, may signal the presence of the PTC to the 5'end of the transcript, resulting in decapping and rapid exonucleolytic digestion of the mRNA. In the NSD pathway, which targets mRNAs lacking termination codons, the ribosome is believed to translate through the 3' untranslated region and stall at the end of the poly(A) tail. NSD involves an eRF3-like protein, Ski7p, which is hypothesized to bind the empty A site of the ribosome and recruit the exosome to degrade the mRNA from the 3' end. NGD targets mRNAs with stalls in translation elongation for endonucleolytic cleavage in a process involving the Dom34 and Hbs1 proteins.
hsa04146	Peroxisome - Homo sapiens (human)	Cellular Processes; Transport and Catabolism	9409:PEX16|8504:PEX3|5824:PEX19|5825:ABCD3|5189:PEX1|5190:PEX6|55670:PEX26|5191:PEX7|5830:PEX5|5195:PEX14|5194:PEX13|5193:PEX12|5192:PEX10|5828:PEX2|5827:PXMP2|4358:MPV17|255027:MPV17L|11264:PXMP4|8800:PEX11A|8799:PEX11B|92960:PEX11G|10478:SLC25A17|26061:HACL1|23600:AMACR|5264:PHYH|8310:ACOX3|51:ACOX1|8309:ACOX2|3295:HSD17B4|6342:SCP2|570:BAAT|1962:EHHADH|30:ACAA1|26063:DECR2|1891:ECH1|215:ABCD1|225:ABCD2|5826:ABCD4|11001:SLC27A2|2180:ACSL1|2182:ACSL4|2181:ACSL3|51703:ACSL5|23305:ACSL6|55825:PECR|10455:ECI2|83594:NUDT12|390916:NUDT19|10005:ACOT8|1384:CRAT|54677:CROT|23417:MLYCD|8443:GNPAT|8540:AGPS|55711:FAR2|84188:FAR1|4598:MVK|10654:PMVK|189:AGXT|1610:DAO|8528:DDO|3418:IDH2|3417:IDH1|196743:PAOX|51268:PIPOX|3155:HMGCL|51179:HAO2|54363:HAO1|847:CAT|25824:PRDX5|6647:SOD1|6648:SOD2|4843:NOS2|5052:PRDX1|2053:EPHX2|373156:GSTK1|7498:XDH|10901:DHRS4	Refsum disease|Adrenoleukodystrophy (ALD)|Acatalasia|Zellweger syndrome spectrum|Rhizomelic chondrodysplasia punctata|Peroxisomal beta-oxidation enzyme deficiency|Congenital bile acid synthesis defect (CBAS)|Leukoencephalopathy with dystonia and motor neuropathy|Roussy-Levy syndrome	Febuxostat (JAN/USAN/INN)|Oxypurinol (USAN)|Allopurinol sodium	Peroxisomes are essential organelles that play a key role in redox signalling and lipid homeostasis. They contribute to many crucial metabolic processes such as fatty acid oxidation, biosynthesis of ether lipids and free radical detoxification. The biogenesis of peroxisomes starts with the early peroxins PEX3, PEX16 and PEX19 and proceeds via several steps. The import of membrane proteins into peroxisomes needs PEX19 for recognition, targeting and insertion via docking at PEX3. Matrix proteins in the cytosol are recognized by peroxisomal targeting signals (PTS) and transported to the docking complex at the peroxisomal membrane. Peroxisomes' deficiencies lead to severe and often fatal inherited peroxisomal disorders (PD). PDs are usually classified in two groups. The first group is disorders of peroxisome biogenesis which include Zellweger syndrome, and the second group is single peroxisomal enzyme deficiencies.
hsa05410	Hypertrophic cardiomyopathy (HCM) - Homo sapiens (human)	Human Diseases; Cardiovascular Diseases	3672:ITGA1|3673:ITGA2|3674:ITGA2B|3675:ITGA3|3676:ITGA4|3678:ITGA5|3655:ITGA6|3679:ITGA7|8516:ITGA8|3680:ITGA9|8515:ITGA10|22801:ITGA11|3685:ITGAV|3688:ITGB1|3690:ITGB3|3691:ITGB4|3693:ITGB5|3694:ITGB6|3695:ITGB7|3696:ITGB8|6444:SGCD|6445:SGCG|6442:SGCA|6443:SGCB|1605:DAG1|1674:DES|1756:DMD|60:ACTB|71:ACTG1|7273:TTN|7139:TNNT2|7134:TNNC1|7137:TNNI3|70:ACTC1|7168:TPM1|7169:TPM2|7170:TPM3|7171:TPM4|4607:MYBPC3|4634:MYL3|4633:MYL2|2010:EMD|4000:LMNA|775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|782:CACNB1|783:CACNB2|784:CACNB3|785:CACNB4|781:CACNA2D1|9254:CACNA2D2|55799:CACNA2D3|93589:CACNA2D4|786:CACNG1|10369:CACNG2|10368:CACNG3|27092:CACNG4|27091:CACNG5|59285:CACNG6|59284:CACNG7|59283:CACNG8|6262:RYR2|5562:PRKAA1|5563:PRKAA2|5565:PRKAB2|5564:PRKAB1|5571:PRKAG1|53632:PRKAG3|51422:PRKAG2|1636:ACE|3479:IGF1|7040:TGFB1|7042:TGFB2|7043:TGFB3|7124:TNF|3569:IL6|3908:LAMA2|4624:MYH6|4625:MYH7|488:ATP2A2|6546:SLC8A1	Hypertrophic cardiomyopathy (HCM)|Brugada syndrome (BRS)|Wolff-Parkinson-White (WPW) syndrome		Hypertrophic cardiomyopathy (HCM) is a primary myocardial disorder with an autosomal dominant pattern of inheritance that is characterized by hypertrophy of the left ventricles with histological features of myocyte hypertrophy, myfibrillar disarray, and interstitial fibrosis. HCM is one of the most common inherited cardiac disorders, with a prevalence in young adults of 1 in 500. Hundreds of mutations in 11 genes that encode protein constituents of the sarcomere have been identified in HCM. These mutations increase the Ca2+ sensitivity of cardiac myofilaments. Increased myofilament Ca2+ sensitivity is expected to increase the ATP utilization by actomyosin at submaximal Ca2+ concentrations, which might cause an imbalance in energy supply and demand in the heart under severe stress. The inefficient use of ATP suggests that an inability to maintain normal ATP levels could be the central abnormality. This theory might be supported by the discovery of the role of a mutant PRKAG2 gene in HCM, which in active form acts as a central sensing mechanism protecting cells from depletion of ATP supplies. The increase in the myfilament Ca2+ sensitivity well account for the diastolic dysfunction of model animals as well as human patients of HCM. It has been widely proposed that left ventricular hypertrophy is not a primary manifestation but develops as compensatory response to sarcomere dysfunction.
hsa00601	Glycosphingolipid biosynthesis - lacto and neolacto series - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	84002:B3GNT5|8708:B3GALT1|8707:B3GALT2|10317:B3GALT5|2524:FUT2|2523:FUT1|2525:FUT3|6487:ST3GAL3|6484:ST3GAL4|28:ABO|2683:B4GALT1|8704:B4GALT2|8703:B4GALT3|8702:B4GALT4|10690:FUT9|2526:FUT4|2527:FUT5|2528:FUT6|2529:FUT7|10402:ST3GAL6|6489:ST8SIA1|10678:B3GNT2|11041:B3GNT1|10331:B3GNT3|79369:B3GNT4|2651:GCNT2	Nonsyndromic autosomal recessive mental retardation (NS-ARMR)|Adult i phenotype		
hsa05020	Prion diseases - Homo sapiens (human)	Human Diseases; Neurodegenerative Diseases	5621:PRNP|3309:HSPA5|4685:NCAM2|4684:NCAM1|3915:LAMC1|6647:SOD1|10963:STIP1|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|581:BAX|2534:FYN|727:C5|729:C6|730:C7|731:C8A|732:C8B|733:C8G|735:C9|712:C1QA|713:C1QB|714:C1QC|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|2002:ELK1|1958:EGR1|6352:CCL5|3552:IL1A|3553:IL1B|3569:IL6|3303:HSPA1A|4851:NOTCH1	Prion diseases		Prion diseases, also termed transmissible spongiform encephalopathies (TSEs), are a group of fatal neurodegenerative diseases that affect humans and a number of other animal species. The etiology of these diseases is thought to be associated with the conversion of a normal protein, PrPC, into an infectious, pathogenic form, PrPSc. The conversion is induced by prion infections (for example, variant Creutzfeldt-Jakob disease (vCJD), iatrogenic CJD, Kuru), mutations (familial CJD, Gerstmann-Straussler-Scheinker syndrome, fatal familial insomnia (FFI)) or unknown factors (sporadic CJD (sCJD)), and is thought to occur after PrPC has reached the plasma membrane or is re-internalized for degradation. The PrPSc form shows greater protease resistance than PrPC and accumulates in affected individuals, often in the form of extracellular plaques. Pathways that may lead to neuronal death comprise oxidative stress, regulated activation of complement, ubiquitin-proteasome and endosomal-lysosomal systems, synaptic alterations and dendritic atrophy, corticosteroid response, and endoplasmic reticulum stress. In addition, the conformational transition could lead to the lost of a beneficial activity of the natively folded protein, PrPC.
hsa03410	Base excision repair - Homo sapiens (human)	Genetic Information Processing; Replication and Repair	4968:OGG1|4913:NTHL1|79661:NEIL1|252969:NEIL2|55247:NEIL3|7374:UNG|6996:TDG|23583:SMUG1|4595:MUTYH|4350:MPG|8930:MBD4|328:APEX1|27301:APEX2|5423:POLB|27343:POLL|3146:HMGB1|7515:XRCC1|3980:LIG3|143:PARP4|10039:PARP3|10038:PARP2|142:PARP1|5111:PCNA|5424:POLD1|5425:POLD2|10714:POLD3|57804:POLD4|5426:POLE|5427:POLE2|54107:POLE3|56655:POLE4|2237:FEN1|3978:LIG1	Familial adenomatous polyposis	Iniparib (USAN/INN)	Base excision repair (BER) is the predominant DNA damage repair pathway for the processing of small base lesions, derived from oxidation and alkylation damages. BER is normally defined as DNA repair initiated by lesion-specific DNA glycosylases and completed by either of the two sub-pathways: short-patch BER where only one nucleotide is replaced and long-patch BER where 2-13 nucleotides are replaced. Each sub-pathway of BER relies on the formation of protein complexes that assemble at the site of the DNA lesion and facilitate repair in a coordinated fashion. This process of complex formation appears to provide an increase in specificity and efficiency to the BER pathway, thereby facilitating the maintenance of genome integrity by preventing the accumulation of highly toxic repair intermediates.
hsa04730	Long-term depression - Homo sapiens (human)	Organismal Systems; Nervous System	4842:NOS1|2982:GUCY1A3|2977:GUCY1A2|2983:GUCY1B3|5593:PRKG2|5592:PRKG1|10842:PPP1R17|5518:PPP2R1A|5519:PPP2R1B|5516:PPP2CB|5515:PPP2CA|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|2895:GRID2|2911:GRM1|2915:GRM5|2773:GNAI3|2770:GNAI1|2771:GNAI2|2775:GNAO1|2781:GNAZ|2778:GNAS|2768:GNA12|10672:GNA13|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|5579:PRKCB|5578:PRKCA|5582:PRKCG|2776:GNAQ|2767:GNA11|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|2890:GRIA1|2891:GRIA2|2892:GRIA3|4067:LYN|773:CACNA1A|3708:ITPR1|3709:ITPR2|3710:ITPR3|6261:RYR1|1392:CRH|1394:CRHR1|3479:IGF1|3480:IGF1R	Spinocerebellar ataxia (SCA)|Syndromic X-linked mental retardation with epilepsy or seizures|Central core disease|Episodic ataxias|Familial or sporadic hemiplegic migraine|Neurodegeneration with brain iron accumulation (NBIA)	Topiramate (JAN/USAN/INN)|Talampanel (INN)|Corticorelin acetate (USAN)|Corticorelin ovine triflutate (USAN)|Corticorelin (human) (JAN)|Fenobam (USAN)	Cerebellar long-term depression (LTD), thought to be a molecular and cellular basis for cerebellar learning, is a process involving a decrease in the synaptic strength between parallel fiber (PF) and Purkinje cells (PCs) induced by the conjunctive activation of PFs and climbing fiber (CF). Multiple signal transduction pathways have been shown to be involved in this process. Activation of PFs terminating on spines in dendritic branchlets leads to glutamate release and activation of both AMPA and mGluRs. Activation of CFs, which make multiple synaptic contacts on proximal dendrites, also via AMPA receptors, opens voltage-gated calcium channels (VGCCs) and causes a generalized influx of calcium. These cellular signals, generated from two different synaptic origins, trigger a cascade of events culminating in a phosphorylation-dependent, long-term reduction in AMPA receptor sensitivity at the PF-PC synapse. This may take place either through receptor internalization and/or through receptor desensitization.
hsa04622	RIG-I-like receptor signaling pathway - Homo sapiens (human)	Organismal Systems; Immune System	23586:DDX58|64135:IFIH1|57506:MAVS|79132:DHX58|7187:TRAF3|10010:TANK|64343:AZI2|9755:TBKBP1|8517:IKBKG|29110:TBK1|9641:IKBKE|3661:IRF3|3665:IRF7|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3456:IFNB1|3467:IFNW1|338376:IFNE|56832:IFNK|8717:TRADD|8772:FADD|8737:RIPK1|841:CASP8|843:CASP10|1147:CHUK|3551:IKBKB|4793:NFKBIB|4792:NFKBIA|4790:NFKB1|5970:RELA|7186:TRAF2|6885:MAP3K7|7189:TRAF6|4214:MAP3K1|5602:MAPK10|5601:MAPK9|5599:MAPK8|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|3576:IL8|7124:TNF|3592:IL12A|3593:IL12B|3627:CXCL10|7706:TRIM25|1540:CYLD|54941:RNF125|9636:ISG15|9474:ATG5|9140:ATG12|79671:NLRX1|340061:TMEM173|55593:OTUD5|80143:SIKE1|1654:DDX3X|8653:DDX3Y|5300:PIN1|26007:DAK	Brooke-Spiegler syndrome|Cocoon syndrome		Specific families of pattern recognition receptors are responsible for detecting viral pathogens and generating innate immune responses. Non-self RNA appearing in a cell as a result of intracellular viral replication is recognized by a family of cytosolic RNA helicases termed RIG-I-like receptors (RLRs). The RLR proteins include RIG-I, MDA5, and LGP2 and are expressed in both immune and nonimmune cells. Upon recognition of viral nucleic acids, RLRs recruit specific intracellular adaptor proteins to initiate signaling pathways that lead to the synthesis of type I interferon and other inflammatory cytokines, which are important for eliminating viruses.
hsa00511	Other glycan degradation - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	4758:NEU1|10825:NEU3|4759:NEU2|129807:NEU4|2720:GLB1|3073:HEXA|3074:HEXB|284004:HEXDC|4123:MAN2C1|4125:MAN2B1|23324:MAN2B2|4126:MANBA|64772:ENGASE|2519:FUCA2|2517:FUCA1|175:AGA|2629:GBA	GM2 gangliosidoses|Gaucher disease|alpha-Mannosidosis|beta-Mannosidosis|Fucosidosis|Sialidosis|Aspartylglucosaminuria (AGU)|GM1 gangliosidosis|Progressive myoclonic epilepsy (PME)		
hsa00310	Lysine degradation - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	10157:AASS|501:ALDH7A1|51166:AADAT|55753:OGDHL|4967:OGDH|1743:DLST|2639:GCDH|3030:HADHA|1962:EHHADH|1892:ECHS1|3033:HADH|38:ACAT1|39:ACAT2|51268:PIPOX|55870:ASH1L|84444:DOT1L|10919:EHMT2|79813:EHMT1|64324:NSD1|7468:WHSC1|54904:WHSC1L1|9739:SETD1A|23067:SETD1B|29072:SETD2|80854:SETD7|387893:SETD8|83852:SETDB2|9869:SETDB1|6419:SETMAR|6839:SUV39H1|79723:SUV39H2|51111:SUV420H1|84787:SUV420H2|4297:MLL|8085:MLL2|58508:MLL3|9757:MLL4|55904:MLL5|55217:TMLHE|219:ALDH1B1|224:ALDH3A2|217:ALDH2|223:ALDH9A1|8424:BBOX1|5351:PLOD1|5352:PLOD2|8985:PLOD3|23127:GLT25D2|79709:GLT25D1	Glutaric acidemia|Hyperlysinemia|Kabuki syndrome|Ehlers-Danlos syndrome (EDS)|Kleefstra syndrome|Nevo syndrome|Lysyl hydroxylase 3 (LH3) deficiency	Cyanamide (JP16)|Disulfiram (JP16/USP/INN)	
hsa00920	Sulfur metabolism - Homo sapiens (human)	Metabolism; Energy Metabolism	9060:PAPSS2|9061:PAPSS1|10380:BPNT1|6818:SULT1A3|6799:SULT1A2|6817:SULT1A1|445329:SULT1A4|6820:SULT2B1|6783:SULT1E1|50515:CHST11|55501:CHST12|166012:CHST13|6821:SUOX|54928:IMPAD1	SEMD, Pakistani type		
hsa05414	Dilated cardiomyopathy - Homo sapiens (human)	Human Diseases; Cardiovascular Diseases	3672:ITGA1|3673:ITGA2|3674:ITGA2B|3675:ITGA3|3676:ITGA4|3678:ITGA5|3655:ITGA6|3679:ITGA7|8516:ITGA8|3680:ITGA9|8515:ITGA10|22801:ITGA11|3685:ITGAV|3688:ITGB1|3690:ITGB3|3691:ITGB4|3693:ITGB5|3694:ITGB6|3695:ITGB7|3696:ITGB8|6444:SGCD|6445:SGCG|6442:SGCA|6443:SGCB|1605:DAG1|1674:DES|1756:DMD|60:ACTB|71:ACTG1|7273:TTN|7139:TNNT2|7134:TNNC1|7137:TNNI3|70:ACTC1|7168:TPM1|7169:TPM2|7170:TPM3|7171:TPM4|4607:MYBPC3|4634:MYL3|4633:MYL2|2010:EMD|4000:LMNA|100132941:uncharacterized|100291917:uncharacterized|153:ADRB1|2778:GNAS|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|782:CACNB1|783:CACNB2|784:CACNB3|785:CACNB4|781:CACNA2D1|9254:CACNA2D2|55799:CACNA2D3|93589:CACNA2D4|786:CACNG1|10369:CACNG2|10368:CACNG3|27092:CACNG4|27091:CACNG5|59285:CACNG6|59284:CACNG7|59283:CACNG8|6262:RYR2|5350:PLN|3479:IGF1|7040:TGFB1|7042:TGFB2|7043:TGFB3|7124:TNF|3908:LAMA2|4624:MYH6|4625:MYH7|488:ATP2A2|6546:SLC8A1	Dilated cardiomyopathy (DCM)|Brugada syndrome (BRS)		Dilated cardiomyopathy (DCM) is a heart muscle disease characterised by dilation and impaired contraction of the left or both ventricles that results in progressive heart failure and sudden cardiac death from ventricular arrhythmia. Genetically inherited forms of DCM ("familial" DCM) have been identified in 25-35% of patients presenting with this disease, and the inherited gene defects are an important cause of "familial" DCM. The pathophysiology may be separated into two categories: defects in force generation and defects in force transmission. In cases where an underlying pathology cannot be identified, the patient is diagnosed with an "idiopathic" DCM. Current hypotheses regarding causes of "idiopathic" DCM focus on myocarditis induced by enterovirus and subsequent autoimmune myocardium impairments. Antibodies to the beta1-adrenergic receptor (beta1AR), which are detected in a substantial number of patients with "idiopathic" DCM,  may increase the concentration of intracellular cAMP and intracellular Ca2+, a condition often leading to a transient hyper-performance of the heart followed by depressed heart function and heart failure.
hsa00533	Glycosaminoglycan biosynthesis - keratan sulfate - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	2530:FUT8|2683:B4GALT1|8704:B4GALT2|8703:B4GALT3|10678:B3GNT2|11041:B3GNT1|4166:CHST6|8702:B4GALT4|93010:B3GNT7|8534:CHST1|6487:ST3GAL3|9435:CHST2|10164:CHST4|6482:ST3GAL1|6483:ST3GAL2	Nonsyndromic autosomal recessive mental retardation (NS-ARMR)|Macular corneal dystrophy (MCD)		Keratan sulfate (KS) is a glycosaminoglycan with the basic disaccharide unit of N-acetyllactosamine, Gal(b1-4)GlcNAc(b1-3), with sulfate esters at C-6 of GlcNAc and Gal residues. There are two types of KS distinguished by the protein linkage: type I for N-linked via the N-glycan core structure and type II for O-linked via the O-glycan core 2 structure.
hsa03040	Spliceosome - Homo sapiens (human)	Genetic Information Processing; Transcription	9879:DDX46|7919:DDX39B|8449:DHX16|9785:DHX38|51362:CDC40|8559:PRPF18|1659:DHX8|10569:SLU7|1665:DHX15|6628:SNRPB|6632:SNRPD1|6633:SNRPD2|6634:SNRPD3|6635:SNRPE|6636:SNRPF|6637:SNRPG|6625:SNRNP70|6626:SNRPA|6631:SNRPC|25766:PRPF40B|55660:PRPF40A|58517:RBM25|1655:DDX5|10915:TCERG1|6627:SNRPA1|6629:SNRPB2|10291:SF3A1|8175:SF3A2|10946:SF3A3|23451:SF3B1|10992:SF3B2|23450:SF3B3|10262:SF3B4|83443:SF3B5|51639:SF3B14|84844:PHF5A|11325:DDX42|7307:U2AF1|11338:U2AF2|22827:PUF60|10285:SMNDC1|84991:RBM17|10523:CHERP|23350:U2SURP|57819:LSM2|27258:LSM3|25804:LSM4|23658:LSM5|11157:LSM6|51690:LSM7|51691:NAA38|9129:PRPF3|9128:PRPF4|10465:PPIH|26121:PRPF31|4809:NHP2L1|11017:SNRNP27|10713:USP39|9092:SART1|153527:ZMAT2|84950:PRPF38A|55119:PRPF38B|9343:EFTUD2|23020:SNRNP200|24148:PRPF6|10594:PRPF8|9410:SNRNP40|9416:DDX23|10907:TXNL4A|27339:PRPF19|988:CDC5L|10286:BCAS2|5356:PLRG1|51503:CWC15|56259:CTNNBL1|3306:HSPA2|3310:HSPA6|3304:HSPA1B|3305:HSPA1L|3312:HSPA8|3303:HSPA1A|10084:PQBP1|51729:WBP11|22938:SNW1|56949:XAB2|25949:SYF2|51340:CRNKL1|57461:ISY1|51645:PPIL1|10450:PPIE|151903:CCDC12|55696:RBM22|8896:BUD31|9716:AQR|22985:ACIN1|9775:EIF4A3|9939:RBM8A|4116:MAGOH|55110:MAGOHB|9984:THOC1|57187:THOC2|84321:THOC3|10189:ALYREF|4686:NCBP1|22916:NCBP2|3178:HNRNPA1|144983:HNRNPA1L2|220988:HNRNPA3|3183:HNRNPC|27316:RBMX|494115:RBMXL1|3190:HNRNPK|4670:HNRNPM|3192:HNRNPU|5093:PCBP1|8683:SRSF9|6426:SRSF1|6427:SRSF2|10929:SRSF8|6428:SRSF3|6430:SRSF5|6429:SRSF4|6431:SRSF6|6432:SRSF7|29896:TRA2A|6434:TRA2B|10772:SRSF10	Retinitis pigmentosa (RP)		After transcription, eukaryotic mRNA precursors contain protein-coding exons and noncoding introns. In the following splicing, introns are excised and exons are joined by a macromolecular complex, the spliceosome. The standard spliceosome is made up of five small nuclear ribonucleoproteins (snRNPs), U1, U2, U4, U5, and U6 snRNPs, and several spliceosome-associated proteins (SAPs). Spliceosomes are not a simple stable complex, but a dynamic family of particles that assemble on the mRNA precursor and help fold it into a conformation that allows transesterification to proceed. Various spliceosome forms (e.g. A-, B- and C-complexes) have been identified.
hsa02010	ABC transporters - Homo sapiens (human)	Environmental Information Processing; Membrane Transport	19:ABCA1|20:ABCA2|21:ABCA3|24:ABCA4|10347:ABCA7|26154:ABCA12|154664:ABCA13|23461:ABCA5|23460:ABCA6|10351:ABCA8|10350:ABCA9|10349:ABCA10|6890:TAP1|6891:TAP2|11194:ABCB8|23457:ABCB9|23456:ABCB10|5243:ABCB1|5244:ABCB4|340273:ABCB5|10058:ABCB6|22:ABCB7|8647:ABCB11|4363:ABCC1|1244:ABCC2|8714:ABCC3|10057:ABCC5|368:ABCC6|6833:ABCC8|10060:ABCC9|85320:ABCC11|94160:ABCC12|10257:ABCC4|1080:CFTR|89845:ABCC10|215:ABCD1|225:ABCD2|5825:ABCD3|5826:ABCD4|9619:ABCG1|64137:ABCG4|9429:ABCG2|64240:ABCG5|64241:ABCG8	Sitosterolemia|Tangier disease|Adrenoleukodystrophy (ALD)|Hyperbilirubinemia|Pulmonary surfactant metabolism dysfunction (SMDP)|Cystic fibrosis (CF)|Pseudoxanthoma elasticum|Familial cholestasis|Harlequin ichthyosis|Lamellar ichthyosis (LI) and Non-bullous congenital ichthyosiform erythroderma (NBCIE)|Stargardt disease (STGD)|Macular degeneration|Hypoalphalipoproteinemia|Bare lymphocyte syndrome (BLS) type1|Congenital bilateral absence of vas deferens	Acetohexamide (JP16/USP/INN)|Chlorpropamide (JP16/USP/INN)|Diazoxide (JAN/USP/INN)|Glipizide (USP/INN)|Glibenclamide (JP16/INN)|Tolazamide (JP16/USP/INN)|Tolbutamide (JP16/USP/INN)|Minoxidil (JAN/USP/INN)|Glimepiride (JP16/USP/INN)|Repaglinide (JAN/USP/INN)|Nateglinide (JP16/USAN/INN)|Glymidine sodium (JAN/USAN/INN)|Gliclazide (JP16/INN)|Glyclopyramide (JAN/INN)|Nicorandil (JP16/USAN/INN)|Mitiglinide calcium hydrate (JAN)|Levcromakalim (USAN/INN)|Carbutamide (INN)|Glibornuride (USAN/INN)|Gliquidone (INN)|Pinacidil (USAN)|Tolbutamide sodium, sterile|Metahexamide (INN)|Glisoxepide (INN)	The ATP-binding cassette (ABC) transporters form one of the largest known protein families, and are widespread in bacteria, archaea, and eukaryotes. They couple ATP hydrolysis to active transport of a wide variety of substrates such as ions, sugars, lipids, sterols, peptides, proteins, and drugs. The structure of a prokaryotic ABC transporter usually consists of three components; typically two integral membrane proteins each having six transmembrane segments, two peripheral proteins that bind and hydrolyze ATP, and a periplasmic (or lipoprotein) substrate-binding protein. Many of the genes for the three components form operons as in fact observed in many bacterial and archaeal genomes. On the other hand, in a typical eukaryotic ABC transporter, the membrane spanning protein and the ATP-binding protein are fused, forming a multi-domain protein with the membrane-spanning domain (MSD) and the nucleotide-binding domain (NBD).
hsa05416	Viral myocarditis - Homo sapiens (human)	Human Diseases; Cardiovascular Diseases	1525:CXADR|1604:CD55|2534:FYN|857:CAV1|25:ABL1|27:ABL2|5879:RAC1|5880:RAC2|5881:RAC3|6444:SGCD|6445:SGCG|6442:SGCA|6443:SGCB|1605:DAG1|1756:DMD|60:ACTB|71:ACTG1|8672:EIF4G3|1982:EIF4G2|1981:EIF4G1|595:CCND1|841:CASP8|637:BID|54205:CYCS|842:CASP9|836:CASP3|22989:MYH15|4622:MYH4|8735:MYH13|4629:MYH11|4620:MYH2|4621:MYH3|4619:MYH1|4626:MYH8|4625:MYH7|4628:MYH10|57644:MYH7B|4627:MYH9|79784:MYH14|4624:MYH6|959:CD40LG|958:CD40|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|3133:HLA-E|3134:HLA-F|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|941:CD80|942:CD86|940:CD28|5551:PRF1|3683:ITGAL|3689:ITGB2|3383:ICAM1|100132941:uncharacterized|100291917:uncharacterized|3908:LAMA2	Viral myocarditis		Myocarditis is a cardiac disease associated with inflammation and injury of the myocardium. It results from various etiologies, both noninfectious and infectious, but coxsackievirus B3 (CVB3) is still considered the dominant etiological agent. Myocarditis may be caused by direct cytopathic effects of virus, a pathologic immune response to persistent virus, or autoimmunity triggered by the viral infection. The virus enters the myocyte through internalization of the coxsackie-adenoviral receptor (CAR) and its coreceptor, decay-accelerating factor (DAF). Viral proteases cleave various proteins in the host cell. One example is viral protease 2A, which cleaves eukaryote initiation factor 4G (eIF4G) and the dystrophin protein, resulting in a complete shutdown of cap-dependent RNA translation and cytoskeletal destruction in infected cardiomyocytes, respectively. CVB3 also cleaves the member of the Bcl-2 family Bid, leading to apoptosis. CVB3 infection also induces the cleavage of cyclin D protein through a proteasome-dependent pathway, leading to the host cell-growth arrest. Viral infection and necrosis of myocytes may lead to the release of intracellular antigens, resulting in activation of self-reactive T cells. CVB infection is a significant cause of dilated cardiomyopathy (DCM) as well as myocarditis. Epidemiologically, myocarditis underlies a significant portion of patients with DCM.
hsa05332	Graft-versus-host disease - Homo sapiens (human)	Human Diseases; Immune Diseases	3569:IL6|3552:IL1A|3553:IL1B|7124:TNF|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|941:CD80|942:CD86|940:CD28|3558:IL2|3133:HLA-E|3134:HLA-F|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|356:FASLG|355:FAS|5551:PRF1|3002:GZMB|3458:IFNG|3824:KLRD1|3802:KIR2DL1|3803:KIR2DL2|3804:KIR2DL3|3811:KIR3DL1|3812:KIR3DL2|3821:KLRC1|57292:KIR2DL5A	Graft-versus-host disease		Graft-versus-host disease (GVHD) is a lethal complication of allogeneic hematopoietic stem cell transplantation (HSCT) where immunocompetent donor T cells attack the genetically disparate host cells. GVHD pathophysiology can be summerized in a three-step process. Step 1 involves the development of an inflammatory milieu resulting from damage in the host tissues induced by the preparative chemotherapy or radiotherapy regimen. Damaged tissues secrete inflammatory cytokines, including interleukin 1 (IL-1), and tumor necrosis factor (TNF-alpha ). During step 2, antigen-presenting cells (APCs) trigger the activation of donor-derived T cells, which induce further T-cell expansion, induce cytotoxic T lymphocytes (CTL) and natural killer (NK) cells responses and prime additional mononuclear phagocytes to produce TNF-alpha and IL-1. Also, nitric oxide (NO) is produced by activated macrophages, and it may contribute to the tissue damage seen during step 3. During step 3, the effector phase, activated CTL and NK cells mediate cytotoxicity against target host cells through Fas-Fas ligand interactions and perforin-granzyme B.
hsa04660	T cell receptor signaling pathway - Homo sapiens (human)	Organismal Systems; Immune System	915:CD3D|916:CD3E|917:CD3G|919:CD247|920:CD4|925:CD8A|926:CD8B|5788:PTPRC|3932:LCK|2534:FYN|7535:ZAP70|3937:LCP2|27040:LAT|3702:ITK|7006:TEC|8440:NCK2|4690:NCK1|10451:VAV3|7409:VAV1|7410:VAV2|9402:GRAP2|2885:GRB2|5058:PAK1|5062:PAK2|5063:PAK3|10298:PAK4|56924:PAK6|57144:PAK7|387:RHOA|998:CDC42|1739:DLG1|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|4776:NFATC4|4772:NFATC1|4773:NFATC2|4775:NFATC3|10725:NFAT5|6654:SOS1|6655:SOS2|10125:RASGRP1|3265:HRAS|3845:KRAS|4893:NRAS|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|2353:FOS|3725:JUN|84433:CARD11|8915:BCL10|10892:MALT1|6885:MAP3K7|5609:MAP2K7|1147:CHUK|3551:IKBKB|8517:IKBKG|4790:NFKB1|5970:RELA|4792:NFKBIA|4793:NFKBIB|4794:NFKBIE|940:CD28|29851:ICOS|959:CD40LG|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|5163:PDK1|207:AKT1|208:AKT2|10000:AKT3|1326:MAP3K8|9020:MAP3K14|2932:GSK3B|5133:PDCD1|1493:CTLA4|5777:PTPN6|23624:CBLC|868:CBLB|867:CBL|3558:IL2|3565:IL4|3567:IL5|3586:IL10|3458:IFNG|1437:CSF2|7124:TNF|1019:CDK4|5335:PLCG1|5588:PRKCQ|5601:MAPK9	Type I diabetes mellitus|Osteoporosis, lymphedema, anhydrotic ectodermal dysplasia with immunodeficiency (OLEDAID)|Incontinentia pigmenti|Cocoon syndrome	Tacrolimus hydrate (JP16)|Ciclosporin (JP16)|Ipilimumab (USAN/INN)|Muromonab-CD3 (JAN/USAN/INN)|Pimecrolimus (JAN/USAN/INN)|Tacrolimus (INN)|Catumaxomab (INN)	Activation of T lymphocytes is a key event for an efficient response of the immune system. It requires the involvement of the T-cell receptor (TCR) as well as costimulatory molecules such as CD28. Engagement of these receptors through the interaction with a foreign antigen associated with major histocompatibility complex molecules and CD28 counter-receptors B7.1/B7.2, respectively, results in a series of signaling cascades. These cascades comprise an array of protein-tyrosine kinases, phosphatases, GTP-binding proteins and adaptor proteins that regulate generic and specialised functions, leading to T-cell proliferation, cytokine production and differentiation into effector cells.
hsa04620	Toll-like receptor signaling pathway - Homo sapiens (human)	Organismal Systems; Immune System	7096:TLR1|7097:TLR2|10333:TLR6|3929:LBP|929:CD14|23643:LY96|7098:TLR3|7099:TLR4|7100:TLR5|51284:TLR7|51311:TLR8|1513:CTSK|54106:TLR9|5879:RAC1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|54472:TOLLIP|4615:MYD88|114609:TIRAP|8772:FADD|841:CASP8|51135:IRAK4|3654:IRAK1|7189:TRAF6|10454:TAB1|23118:TAB2|6885:MAP3K7|8517:IKBKG|1147:CHUK|3551:IKBKB|4792:NFKBIA|4790:NFKB1|5970:RELA|1326:MAP3K8|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|5606:MAP2K3|5608:MAP2K6|6416:MAP2K4|5609:MAP2K7|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|5602:MAPK10|5601:MAPK9|5599:MAPK8|3725:JUN|2353:FOS|7124:TNF|3553:IL1B|3569:IL6|3592:IL12A|3593:IL12B|3576:IL8|6352:CCL5|353376:TICAM2|148022:TICAM1|8737:RIPK1|3663:IRF5|3665:IRF7|6696:SPP1|9641:IKBKE|29110:TBK1|7187:TRAF3|3661:IRF3|958:CD40|941:CD80|942:CD86|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3456:IFNB1|3454:IFNAR1|3455:IFNAR2|6772:STAT1|3627:CXCL10|4283:CXCL9|6373:CXCL11|6348:CCL3|6351:CCL4	Defects of toll-like receptor signaling|Pycnodysostosis|Leprosy|Pyogenic bacterial infections, recurrent, due to MYD88 deficiency|Macular degeneration|Cocoon syndrome|Chronic Mucocutaneous Candidiasis (CMC)	Interferon alfa-2a (genetical recombination) (JAN)|Interferon beta-1b (genetical recombination) (JAN)|Imiquimod (JAN/USAN/INN)|Interferon alfacon-1 (genetical recombination) (JAN)|Interferon alfa-2b (genetical recombination) (JAN)|Peginterferon alfa-2a (genetical recombination) (JAN)|Peginterferon alfa-2b (generical recombination) (JAN)|Abatacept (genetical recombination) (JAN)|Interferon beta (JAN)|Interferon alfa (BALL-1) (JAN)|Certolizumab pegol (genetical recombination) (JAN)|Eritoran tetrasodium (USAN)|Galiximab (USAN/INN)|Interferon alfa-n1 (USAN)|Interferon beta-1a (genetical recombination) (JAN)|Isatoribine (USAN)|Loxoribine (USAN/INN)|Relacatib (USAN/INN)|Rilonacept (USAN/INN)|Albinterferon alfa-2b (USAN)|Eritoran sodium (JAN)	Specific families of pattern recognition receptors are responsible for detecting microbial pathogens and generating innate immune responses. Toll-like receptors (TLRs) are membrane-bound receptors identified as homologs of Toll in Drosophila. Mammalian TLRs are expressed on innate immune cells, such as macrophages and dendritic cells, and respond to the membrane components of Gram-positive or Gram-negative bacteria. Pathogen recognition by TLRs provokes rapid activation of innate immunity by inducing production of proinflammatory cytokines and upregulation of costimulatory molecules. TLR signaling pathways are separated into two groups: a MyD88-dependent pathway that leads to the production of proinflammatory cytokines with quick activation of NF-{kappa}B and MAPK, and a MyD88-independent pathway associated with the induction of IFN-beta and IFN-inducible genes, and maturation of dendritic cells with slow activation of NF-{kappa}B and MAPK.
hsa00603	Glycosphingolipid biosynthesis - globo series - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	53947:A4GALT|2717:GLA|8706:B3GALNT1|3073:HEXA|3074:HEXB|10317:B3GALT5|26301:GBGT1|4668:NAGA|2524:FUT2|2523:FUT1|6482:ST3GAL1|6483:ST3GAL2|6489:ST8SIA1|10690:FUT9	GM2 gangliosidoses|Fabry disease|Alpha-N-acetylgalactosaminidase deficiency		
hsa04971	Gastric acid secretion - Homo sapiens (human)	Organismal Systems; Digestive System	1131:CHRM3|2520:GAST|887:CCKBR|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|5579:PRKCB|5578:PRKCA|5582:PRKCG|7430:EZR|3708:ITPR1|3709:ITPR2|3710:ITPR3|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|4638:MYLK|85366:MYLK2|91807:MYLK3|3274:HRH2|2778:GNAS|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|6750:SST|6752:SSTR2|2773:GNAI3|2770:GNAI1|2771:GNAI2|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|495:ATP4A|496:ATP4B|9992:KCNE2|3784:KCNQ1|3758:KCNJ1|3759:KCNJ2|3766:KCNJ10|3772:KCNJ15|3773:KCNJ16|1080:CFTR|3776:KCNK2|54207:KCNK10|476:ATP1A1|480:ATP1A4|478:ATP1A3|477:ATP1A2|481:ATP1B1|482:ATP1B2|483:ATP1B3|23439:ATP1B4|6548:SLC9A1|389015:SLC9A4|115111:SLC26A7|6522:SLC4A2|60:ACTB|760:CA2	Hereditary pancreatitis	Atropine (USP)|Scopolamine (INN)|Hyoscyamine (USP)|Methyloctatropine bromide (JAN)|Cimetidine (JP16/USP/INN)|Famotidine (JP16/USP/INN)|Lansoprazole (JAN/USP/INN)|Tropicamide (JP16/USP/INN)|Ranitidine (USAN/INN)|Nizatidine (JP16/USP/INN)|Omeprazole (JP16/USP/INN)|Oxybutynin (USAN/INN)|Propantheline bromide (JP16/USP/INN)|Carbachol (JAN/USP/INN)|Pilocarpine (JAN/USP)|Glycopyrronium bromide (JAN/INN)|Tolterodine (USAN/INN)|Cevimeline hydrochloride hydrate (JAN)|Ranitidine hydrochloride (JP16/USP)|Hyoscine methobromide (INN)|Hyoscyamine sulfate (USP)|Mepenzolate bromide (JP16/INN)|Methanthelinium bromide (INN)|Oxybutynin hydrochloride (JAN)|Tridihexethyl chloride (BAN)|Sodium rabeprazole (JP16)|Orphenadrine citrate (USP)|Benztropine mesilate (JAN)|Biperiden (JAN/USP/INN)|Procyclidine hydrochloride (USP)|Trihexyphenidyl hydrochloride (JP16/USP)|Chlorpromazine hydrochloride (JP16/USP)|Acetylcholine chloride (JP16/USP/INN)|Bethanechol chloride (JP16/USP)|Cyclopentolate hydrochloride (JP16/USP)|Hexocyclium metilsulfate (INN)|Homatropine hydrobromide (JP16/USP)|Isopropamide iodide (JAN/USP/INN)|Oxyphencyclimine hydrochloride (JAN)|Propiverine hydrochloride (JP16)|Atropine methonitrate (JAN/INN)|Trospium chloride (JAN/USAN/INN)|Profenamine hydrochloride (JAN)|Lafutidine (JAN/INN)|Tolterodine tartrate (JAN/USAN)|Piperidolate hydrochloride (JAN)|Carpronium chloride (JAN/INN)|Tiemonium iodide (JAN/INN)|Omeprazole sodium (USAN)|Piroheptine hydrochloride (JAN)|Solifenacin succinate (JAN/USAN/INN)|Methylbenactyzium bromide (JP16/INN)|Etomidoline (JAN/INN)|Prifinium bromide (JAN/INN)|Scopolamine butylbromide (JP16)|Diponium bromide (JAN/INN)|Roxatidine acetate hydrochloride (JP16/USAN)|Butropium bromide (JP16/INN)|Trimebutine maleate (JP16)|Pipethanate hydrochloride (JAN)|Valethamate bromide (JAN)|Diphenylpiperidinomethyldioxolan iodide (JAN)|Hyoscyamine methylbromide (JAN)|Dalcotidine (JAN/INN)|Darifenacin hydrobromide (JAN/USAN)|Oxapium iodide (JP16/INN)|Proglumide (JP16/USAN/INN)|Panazepide (JAN)|Pibutidine hydrochloride (JAN)|Metixene hydrochloride (JAN)|Tiquizium bromide (JAN/INN)|Tenatoprazole (JAN/INN)|Tiotropium bromide hydrate (JAN)|Oxitropium bromide (JAN/INN)|Aclatonium napadisilate (JAN)|N-Methylscopolamine methylsulfate (JAN)|Esomeprazole magnesium hydrate (JAN)|Pipethanate ethobromide (JAN)|Atropine sulfate (JP16/USP)|Homatropine methylbromide (USP)|Scopolamine hydrobromide hydrate (JP16)|Indium In 111 pentetreotide (USP)|Pilocarpine hydrochloride (JP16/USP)|Ipratropium bromide hydrate (JP16)|Biperiden hydrochloride (JP16/USP)|Biperiden lactate (JAN/USP)|Octreotide acetate (JAN)|Flutropium bromide (JAN)|Timepidium bromide hydrate (JP16)|Pantoprazole Sodium Hydrate (JAN)|Orphenadrine hydrochloride|Devazepide (USAN/INN)|Tarazepide (INN)|Alvameline maleate (USAN)|Atropine oxide hydrochloride (USAN)|Mazaticol hydrochloride hydrate (JAN)|Chlorpromazine hibenzate (JAN)|Profenamine hibenzate (JAN)|Cimetidine hydrochloride (USP)|Darifenacin (USAN/INN)|Dexetimide (USAN/INN)|Atropine methylbromide (JAN)|Donetidine (USAN)|Chlorpromazine phenolphthalinate (JAN)|Esomeprazole sodium (USAN)|Esoxybutynin chloride (USAN)|Ethybenztropine (USAN)|Etintidine hydrochloride (USAN)|Eucatropine hydrochloride (USP XXXII)|Hyoscyamine hydrobromide (USP)|Icotidine (USAN)|Impromidine hydrochloride (USAN)|Lavoltidine succinate (USAN)|Lupitidine hydrochloride (USAN)|Methacholine chloride (USAN/INN)|Metiamide (USAN/INN)|Milameline hydrochloride (USAN)|Omeprazole magnesium (USAN)|Omeprazole sodium injection (JAN)|Oxmetidine hydrochloride (USAN)|Oxmetidine mesylate (USAN)|Pantoprazole (USAN/INN)|Pilocarpine nitrate (USP)|Ranitidine bismuth citrate (USAN)|Timoprazole (INN)|Picoprazole (INN)|Leminoprazole (INN)|Sufotidine (USAN/INN)|Tiotidine (USAN/INN)|Imidafenacin (JAN/INN)|Zaltidine hydrochloride (USAN)|Niperotidine (INN)|Cimetropium bromide (INN)|Choline alfoscerate (INN)|Atropine oxide (INN)|Benzatropine (INN)|Cevimeline (INN)|Cyclopentolate (INN)|Esomeprazole (INN)|Fentonium bromide (INN)|Mazaticol (INN)|Orphenadrine (INN)|Oxyphencyclimine (INN)|Pilocarpine borate|Piperidolate (INN)|Pipethanate (INN)|Piroheptine (INN)|Procyclidine (INN)|Profenamine (INN)|Propiverine (INN)|Rabeprazole (INN)|Roxatidine (INN)|Roxatidine acetate (BAN)|Solifenacin (INN)|Tiemonium methylsulfate|Trihexyphenidyl (INN)|Trimebutine (INN)|Dexlansoprazole (INN/USAN)|Esomeprazole potassium (USAN)|Carpronium chloride hydrate (JAN)	Gastric acid is a key factor in normal upper gastrointestinal functions, including protein digestion and calcium and iron absorption, as well as providing some protection against bacterial infections. The principal stimulants of acid secretion at the level of the parietal cell are histamine (paracrine), gastrin (hormonal), and acetycholine (ACh; neurocrine). Stimulation of acid secretion typically involves an initial elevation of intracellular calcium and cAMP, followed by activation of protein kinase cascades, which trigger the translocation of the proton pump, H+,K+-ATPase, from cytoplasmic tubulovesicles to the apical plasma membrane and thereby H+ secretion into the stomach lumen.
hsa03320	PPAR signaling pathway - Homo sapiens (human)	Organismal Systems; Endocrine System	948:CD36|10999:SLC27A4|376497:SLC27A1|11001:SLC27A2|10998:SLC27A5|28965:SLC27A6|2168:FABP1|2169:FABP2|2170:FABP3|2167:FABP4|2171:FABP5|2172:FABP6|2173:FABP7|5465:PPARA|6256:RXRA|6257:RXRB|6258:RXRG|5467:PPARD|5468:PPARG|335:APOA1|336:APOA2|345:APOC3|116519:APOA5|5360:PLTP|9415:FADS2|6319:SCD|79966:SCD5|1581:CYP7A1|1582:CYP8B1|10062:NR1H3|1593:CYP27A1|1622:DBI|4023:LPL|2180:ACSL1|2182:ACSL4|2181:ACSL3|51703:ACSL5|23305:ACSL6|23205:ACSBG1|81616:ACSBG2|4973:OLR1|1962:EHHADH|1579:CYP4A11|284541:CYP4A22|30:ACAA1|6342:SCP2|8310:ACOX3|51:ACOX1|8309:ACOX2|1375:CPT1B|1374:CPT1A|126129:CPT1C|1376:CPT2|33:ACADL|34:ACADM|51129:ANGPTL4|10580:SORBS1|5346:PLIN1|9370:ADIPOQ|4312:MMP1|7350:UCP1|3611:ILK|5170:PDPK1|7316:UBC|5106:PCK2|5105:PCK1|2712:GK2|2710:GK|364:AQP7|3158:HMGCS2|4199:ME1	Cerebrotendinous xanthomatosis|Hyperlipoproteinemia, type I|Hyperlipoproteinemia, type V|Peroxisomal beta-oxidation enzyme deficiency|Familial partial lipodystrophy (FPL)|Glycerol kinase deficiency (GKD)|Leukoencephalopathy with dystonia and motor neuropathy|Hypoalphalipoproteinemia|Adiponectin deficiency|CD36 deficiency	Clofibrate (JP16/USP/INN)|Gemfibrozil (JAN/USP/INN)|Troglitazone (JAN/USAN/INN)|Fenofibrate (JAN/INN)|Rosiglitazone maleate (JAN/USAN)|Pioglitazone hydrochloride (JP16/USP)|Aluminum clofibrate (JAN/INN)|Bezafibrate (JP16/USAN/INN)|Alitretinoin (USAN)|Bexarotene (USAN/INN)|Ciglitazone (USAN/INN)|Ciprofibrate (USAN/INN)|Darglitazone sodium (USAN)|Ibrolipim (USAN/INN)|Mifobate (USAN/INN)|Muraglitazar (USAN/INN)|Netoglitazone (USAN/INN)|Oxfenicine (USAN/INN)|Rivoglitazone (USAN/INN)|Theofibrate (USAN)|Etofibrate (INN)|Magnesium clofibrate (INN)|pioglitazone (INN)|Rosiglitazone (INN)|Choline fenofibrate (USAN/INN)	Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that are activated by fatty acids and their derivatives. PPAR has three subtypes (PPARalpha, beta/delta, and gamma) showing different expression patterns in vertebrates. Each of them is encoded in a separate gene and binds fatty acids and eicosanoids. PPARalpha plays a role in the clearance of circulating or cellular lipids via the regulation of gene expression involved in lipid metabolism in liver and skeletal muscle. PPARbeta/delta is involved in lipid oxidation and cell proliferation. PPARgamma promotes adipocyte differentiation to enhance blood glucose uptake.
hsa00565	Ether lipid metabolism - Homo sapiens (human)	Metabolism; Lipid Metabolism	8540:AGPS|8611:PPAP2A|8613:PPAP2B|8612:PPAP2C|85465:EPT1|56994:CHPT1|10390:CEPT1|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|151056:PLB1|254531:LPCAT4|133121:ENPP6|5168:ENPP2|5337:PLD1|5338:PLD2|54947:LPCAT2|79888:LPCAT1|5050:PAFAH1B3|5051:PAFAH2|5048:PAFAH1B1|7941:PLA2G7|5049:PAFAH1B2	Rhizomelic chondrodysplasia punctata|Neurodegeneration with brain iron accumulation (NBIA)		
hsa04630	Jak-STAT signaling pathway - Homo sapiens (human)	Environmental Information Processing; Signal Transduction	7173:TPO|2056:EPO|1442:CSH1|2689:GH2|2688:GH1|5617:PRL|3458:IFNG|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3456:IFNB1|3467:IFNW1|56832:IFNK|338376:IFNE|3586:IL10|50604:IL20|11009:IL24|29949:IL19|50616:IL22|55801:IL26|282618:IL29|282616:IL28A|282617:IL28B|3562:IL3|1437:CSF2|3567:IL5|3558:IL2|3565:IL4|3574:IL7|3578:IL9|3600:IL15|59067:IL21|3596:IL13|85480:TSLP|3569:IL6|3592:IL12A|3589:IL11|5008:OSM|3976:LIF|1270:CNTF|23529:CLCF1|1489:CTF1|1440:CSF3|3952:LEP|3593:IL12B|51561:IL23A|3563:IL3RA|1439:CSF2RB|3570:IL6R|3590:IL11RA|9180:OSMR|3977:LIFR|1271:CNTFR|3572:IL6ST|1441:CSF3R|3953:LEPR|3594:IL12RB1|3595:IL12RB2|149233:IL23R|1438:CSF2RA|3568:IL5RA|3559:IL2RA|3560:IL2RB|3561:IL2RG|3566:IL4R|3575:IL7R|3581:IL9R|3601:IL15RA|50615:IL21R|3597:IL13RA1|3598:IL13RA2|64109:CRLF2|2057:EPOR|2690:GHR|5618:PRLR|4352:MPL|3454:IFNAR1|3455:IFNAR2|3459:IFNGR1|3460:IFNGR2|3587:IL10RA|3588:IL10RB|53832:IL20RA|53833:IL20RB|58985:IL22RA1|116379:IL22RA2|163702:IL28RA|3716:JAK1|3717:JAK2|3718:JAK3|7297:TYK2|6772:STAT1|6773:STAT2|6774:STAT3|6775:STAT4|6776:STAT5A|6777:STAT5B|6778:STAT6|10379:IRF9|1387:CREBBP|2033:EP300|8651:SOCS1|8835:SOCS2|9021:SOCS3|122809:SOCS4|9655:SOCS5|30837:SOCS7|1154:CISH|5292:PIM1|4609:MYC|595:CCND1|894:CCND2|896:CCND3|598:BCL2L1|200734:SPRED2|161742:SPRED1|10251:SPRY3|10252:SPRY1|81848:SPRY4|10253:SPRY2|10254:STAM2|8027:STAM|8554:PIAS1|51588:PIAS4|10401:PIAS3|9063:PIAS2|23624:CBLC|868:CBLB|867:CBL|5781:PTPN11|2885:GRB2|6654:SOS1|6655:SOS2|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|5777:PTPN6	Type I diabetes mellitus|PTEN hamartoma tumor syndrome (PHTS)|Growth hormone insensitivity with immunodeficiency|Cold-induced sweating syndrome (CISS) and Crisponi syndrome (CRISPS)|Metachondromatosis|Chronic Mucocutaneous Candidiasis (CMC)|Pulmonary alveolar proteinosis (PAP)	Thiamazole (JP16/INN)|Propylthiouracil (JP16/USP/INN)|Interferon alfa-2a (genetical recombination) (JAN)|Interferon beta-1b (genetical recombination) (JAN)|Interferon gamma-1b (USAN/INN)|Tocilizumab (genetical recombination) (JAN)|Somatropin (genetical recombination) (JAN)|Celmoleukin (genetical recombination) (JP16)|Interferon alfacon-1 (genetical recombination) (JAN)|Interferon alfa-2b (genetical recombination) (JAN)|Peginterferon alfa-2a (genetical recombination) (JAN)|Peginterferon alfa-2b (generical recombination) (JAN)|Teceleukin (genetical recombination) (JP16)|Basiliximab (genetical recombination) (JAN)|Epoetin alfa (genetical recombination) (JAN)|Epoetin beta (genetical recombination) (JAN)|Filgrastim (genetical recombination) (JAN)|Nartograstim (genetical recombination) (JAN)|Lenograstim (genetical recombination) (JAN)|Interferon beta (JAN)|Interferon alfa (BALL-1) (JAN)|Interferon gamma-1a (genetical recombination) (JAN)|Daclizumab (USAN/INN)|Daniplestim (USAN/INN)|Darbepoetin alfa (genetical recombination) (JAN)|Denileukin diftitox (USAN/INN)|Eltrombopag olamine (JAN/USAN)|Epoetin delta (USAN)|Interferon alfa-n1 (USAN)|Interferon beta-1a (genetical recombination) (JAN)|Leridistim (USAN/INN)|Lestaurtinib (USAN/INN)|Pegnartograstim (USAN/INN)|Pegvisomant (genetical recombination) (JAN)|Somatrem (genetical recombination) (JAN)|Pegfilgrastim (INN)|Methylthiouracil (INN)|Benzylthiouracil|Interferon gamma-n1 (JAN)|Albinterferon alfa-2b (USAN)|Romiplostim (genetical recombination) (JAN)|Tofacitinib citrate (JAN/USAN)|Ruxolitinib (USAN/INN)|Ruxolitinib phosphate (JAN/USAN)|Tofacitinib (USAN)	The Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway is one of a handful of pleiotropic cascades used to transduce a multitude of signals for development and homeostasis in animals, from humans to flies. In mammals, the JAK/STAT pathway is the principal signaling mechanism for a wide array of cytokines and growth factors. Following the binding of cytokines to their cognate receptor, STATs are activated by members of the JAK family of tyrosine kinases. Once activated, they dimerize and translocate to the nucleus and modulate the expression of target genes. In addition to the activation of STATs, JAKs mediate the recruitment of other molecules such as the MAP kinases, PI3 kinase etc. These molecules process downstream signals via the Ras-Raf-MAP kinase and PI3 kinase pathways which results in the activation of additional transcription factors.
hsa05152	Tuberculosis - Homo sapiens (human)	Human Diseases; Infectious Diseases	7124:TNF|7132:TNFRSF1A|8717:TRADD|8772:FADD|841:CASP8|843:CASP10|836:CASP3|637:BID|581:BAX|54205:CYCS|842:CASP9|317:APAF1|207:AKT1|208:AKT2|10000:AKT3|572:BAD|596:BCL2|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|3458:IFNG|3459:IFNGR1|3460:IFNGR2|3716:JAK1|3717:JAK2|6772:STAT1|4261:CIITA|5993:RFX5|8625:RFXANK|5994:RFXAP|4800:NFYA|4801:NFYB|4802:NFYC|1385:CREB1|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|972:CD74|1387:CREBBP|2033:EP300|3586:IL10|3587:IL10RA|3588:IL10RB|1520:CTSS|26253:CLEC4E|2207:FCER1G|64581:CLEC7A|6714:SRC|6850:SYK|64170:CARD9|10892:MALT1|8915:BCL10|64127:NOD2|8767:RIPK2|3313:HSPA9|3329:HSPD1|3929:LBP|7097:TLR2|7096:TLR1|10333:TLR6|7099:TLR4|929:CD14|114609:TIRAP|4615:MYD88|51135:IRAK4|3654:IRAK1|3656:IRAK2|7189:TRAF6|4790:NFKB1|5970:RELA|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|5594:MAPK1|5595:MAPK3|5602:MAPK10|5601:MAPK9|5599:MAPK8|4843:NOS2|3569:IL6|3592:IL12A|3593:IL12B|3606:IL18|51561:IL23A|3552:IL1A|3553:IL1B|1051:CEBPB|1054:CEBPG|54106:TLR9|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3456:IFNB1|10332:CLEC4M|30835:CD209|23365:ARHGEF12|387:RHOA|4046:LSP1|1263:PLK3|8844:KSR1|5894:RAF1|7040:TGFB1|7042:TGFB2|7043:TGFB3|1594:CYP27B1|7421:VDR|820:CAMP|718:C3|1378:CR1|3687:ITGAX|3689:ITGB2|3684:ITGAM|4360:MRC1|9902:MRC2|22925:PLA2R1|8877:SPHK1|56848:SPHK2|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|5289:PIK3C3|5868:RAB5A|5869:RAB5B|5878:RAB5C|8411:EEA1|7879:RAB7A|1509:CTSD|535:ATP6V0A1|50617:ATP6V0A4|23545:ATP6V0A2|10312:TCIRG1|9114:ATP6V0D1|245972:ATP6V0D2|51606:ATP6V1H|537:ATP6AP1|527:ATP6V0C|533:ATP6V0B|3920:LAMP2|3916:LAMP1|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|11151:CORO1A|100132941:uncharacterized|100291917:uncharacterized|2209:FCGR1A|2213:FCGR2B|9103:FCGR2C|2212:FCGR2A|2215:FCGR3B|2214:FCGR3A	Tuberculosis		Tuberculosis, or TB, is an infectious disease caused by Mycobacterium tuberculosis. One third of the world's population is thought to be infected with TB. About 90% of those infected result in latent infections, and about 10% of latent infections develop active diseases when their immune system is impaired due to the age, other diseases such as AIDS or exposure to immunosuppressive drugs. TB is transmitted through the air and primarily attacks the lungs, then it can spread by the circulatory system to other parts of body. Once TB bacilli have entered the host by the respiratory route and infected macrophages in the lungs, they interfere with phagosomal maturation, antigen presentation, apoptosis and host immune system to establish persistent or latent infection.
hsa03050	Proteasome - Homo sapiens (human)	Genetic Information Processing; Folding, Sorting and Degradation	5709:PSMD3|5718:PSMD12|5717:PSMD11|9861:PSMD6|5713:PSMD7|5719:PSMD13|10213:PSMD14|5714:PSMD8|7979:SHFM1|5710:PSMD4|5708:PSMD2|5707:PSMD1|5701:PSMC2|5700:PSMC1|5705:PSMC5|5706:PSMC6|5702:PSMC3|5704:PSMC4|5720:PSME1|5721:PSME2|10197:PSME3|23198:PSME4|5687:PSMA6|5683:PSMA2|5685:PSMA4|5688:PSMA7|143471:PSMA8|5686:PSMA5|5682:PSMA1|5684:PSMA3|5694:PSMB6|5695:PSMB7|5691:PSMB3|5690:PSMB2|5693:PSMB5|5689:PSMB1|5692:PSMB4|5698:PSMB9|5699:PSMB10|5696:PSMB8|122706:PSMB11|3458:IFNG|9491:PSMF1|51371:POMP	Keratosis linearis with ichthyosis congenita and sclerosing keratoderma	Bortezomib (JAN/USAN/INN)|Carfilzomib (INN/USAN)	The proteasome is a protein-destroying apparatus involved in many essential cellular functions, such as regulation of cell cycle, cell differentiation, signal transduction pathways, antigen processing for appropriate immune responses, stress signaling, inflammatory responses, and apoptosis. It is capable of degrading a variety of cellular proteins in a rapid and timely fashion and most substrate proteins are modified by ubiquitin before their degradation by the proteasome. The proteasome is a large protein complex consisting of a proteolytic core called the 20S particle and ancillary factors that regulate its activity in various ways. The most common form is the 26S proteasome containing one 20S core particle and two 19S regulatory particles that enable the proteasome to degrade ubiquitinated proteins by an ATP-dependent mechanism. Another form is the immunoproteasome containing two 11S regulatory particles, PA28 alpha and PA28 beta, which are induced by interferon gamma under the conditions of intensified immune response. Other regulatory particles include PA28 gamma and PA200. Although PA28 gamma also belongs to a family of activators of the 20S proteasome, it is localized within the nucleus and forms a homoheptamer. PA28 gamma has been implicated in the regulation of cell cycle progression and apoptosis. PA200 has been identified as a large nuclear protein that stimulates proteasomal hydrolysis of peptides.
hsa05200	Pathways in cancer - Homo sapiens (human)	Human Diseases; Cancers	1630:DCC|836:CASP3|842:CASP9|26060:APPL1|999:CDH1|1499:CTNNB1|1496:CTNNA2|1495:CTNNA1|29119:CTNNA3|8312:AXIN1|8313:AXIN2|10297:APC2|324:APC|2932:GSK3B|6932:TCF7|83439:TCF7L1|6934:TCF7L2|51176:LEF1|332:BIRC5|4609:MYC|595:CCND1|7471:WNT1|7482:WNT2B|7472:WNT2|7473:WNT3|89780:WNT3A|54361:WNT4|7474:WNT5A|81029:WNT5B|7475:WNT6|7477:WNT7B|7476:WNT7A|7479:WNT8B|7478:WNT8A|7483:WNT9A|7484:WNT9B|7480:WNT10B|80326:WNT10A|7481:WNT11|51384:WNT16|8321:FZD1|8324:FZD7|2535:FZD2|7976:FZD3|8322:FZD4|8325:FZD8|7855:FZD5|8323:FZD6|8326:FZD9|11211:FZD10|1856:DVL2|1857:DVL3|1855:DVL1|1284:COL4A2|1286:COL4A4|1288:COL4A6|1287:COL4A5|1282:COL4A1|284217:LAMA1|3908:LAMA2|3911:LAMA5|3909:LAMA3|3910:LAMA4|3912:LAMB1|3913:LAMB2|3914:LAMB3|22798:LAMB4|3915:LAMC1|3918:LAMC2|10319:LAMC3|2335:FN1|3673:ITGA2|3674:ITGA2B|3675:ITGA3|3655:ITGA6|3685:ITGAV|3688:ITGB1|5747:PTK2|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5728:PTEN|4824:NKX3-1|207:AKT1|208:AKT2|10000:AKT3|1147:CHUK|3551:IKBKB|8517:IKBKG|4792:NFKBIA|4790:NFKB1|4791:NFKB2|5970:RELA|5743:PTGS2|4843:NOS2|596:BCL2|330:BIRC3|331:XIAP|329:BIRC2|598:BCL2L1|7185:TRAF1|7186:TRAF2|7187:TRAF3|9618:TRAF4|7188:TRAF5|7189:TRAF6|2475:MTOR|572:BAD|2308:FOXO1|4193:MDM2|7157:TP53|1027:CDKN1B|1026:CDKN1A|613:BCR|25:ABL1|1399:CRKL|1398:CRK|23624:CBLC|868:CBLB|867:CBL|6776:STAT5A|6777:STAT5B|3716:JAK1|6774:STAT3|6772:STAT1|7423:VEGFB|5228:PGF|7422:VEGFA|7424:VEGFC|2277:FIGF|7039:TGFA|1950:EGF|1956:EGFR|2064:ERBB2|5154:PDGFA|5155:PDGFB|5156:PDGFRA|5159:PDGFRB|3479:IGF1|3480:IGF1R|4254:KITLG|3815:KIT|2323:FLT3LG|2322:FLT3|3082:HGF|4233:MET|2258:FGF13|2253:FGF8|8817:FGF18|2257:FGF12|2248:FGF3|2251:FGF6|2256:FGF11|8823:FGF16|2252:FGF7|2259:FGF14|8822:FGF17|9965:FGF19|2254:FGF9|2250:FGF5|2249:FGF4|8074:FGF23|27006:FGF22|26281:FGF20|2255:FGF10|2247:FGF2|26291:FGF21|2246:FGF1|2260:FGFR1|2263:FGFR2|2261:FGFR3|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|3725:JUN|2353:FOS|4312:MMP1|4313:MMP2|4318:MMP9|3576:IL8|1019:CDK4|5979:RET|8030:CCDC6|8031:NCOA4|4914:NTRK1|7170:TPM3|7175:TPR|10342:TFG|11186:RASSF1|83593:RASSF5|6789:STK4|1613:DAPK3|23604:DAPK2|1612:DAPK1|5335:PLCG1|5336:PLCG2|5579:PRKCB|5578:PRKCA|5582:PRKCG|5900:RALGDS|5898:RALA|5899:RALB|10928:RALBP1|998:CDC42|5879:RAC1|5880:RAC2|5881:RAC3|387:RHOA|5602:MAPK10|5601:MAPK9|5599:MAPK8|7849:PAX8|5468:PPARG|6256:RXRA|6257:RXRB|6258:RXRG|5915:RARB|5467:PPARD|3728:JUP|7704:ZBTB16|5371:PML|5914:RARA|861:RUNX1|862:RUNX1T1|6688:SPI1|1050:CEBPA|1438:CSF2RA|1441:CSF3R|1436:CSF1R|3569:IL6|1029:CDKN2A|1871:E2F3|1869:E2F1|1870:E2F2|4149:MAX|8554:PIAS1|51588:PIAS4|10401:PIAS3|9063:PIAS2|1030:CDKN2B|1021:CDK6|1163:CKS1B|6502:SKP2|1017:CDK2|9134:CCNE2|898:CCNE1|5925:RB1|4286:MITF|7040:TGFB1|7042:TGFB2|7043:TGFB3|7046:TGFBR1|7048:TGFBR2|4087:SMAD2|4088:SMAD3|4089:SMAD4|2122:MECOM|1488:CTBP2|1487:CTBP1|3066:HDAC2|3065:HDAC1|4292:MLH1|4436:MSH2|4437:MSH3|2956:MSH6|581:BAX|675:BRCA2|5888:RAD51|356:FASLG|355:FAS|8772:FADD|841:CASP8|637:BID|54205:CYCS|7428:VHL|6921:TCEB1|6923:TCEB2|9978:RBX1|8453:CUL2|112399:EGLN3|112398:EGLN2|54583:EGLN1|2271:FH|3091:HIF1A|2034:EPAS1|405:ARNT|9915:ARNT2|1387:CREBBP|2033:EP300|6513:SLC2A1|6469:SHH|5727:PTCH1|6608:SMO|27148:STK36|51684:SUFU|2737:GLI3|2736:GLI2|2735:GLI1|650:BMP2|652:BMP4|64399:HHIP|8643:PTCH2|367:AR|3320:HSP90AA1|3326:HSP90AB1|7184:HSP90B1|354:KLK3|112401:BIRC8|2113:ETS1|2950:GSTP1|5337:PLD1|79444:BIRC7|8900:CCNA1	von Hippel-Lindau syndrome|Odontoonychodermal dysplasia|Oligodontia-colorectal cancer syndrome|Li-Fraumeni syndrome|Basal cell nevus syndrome|Pilomatricoma|Choroid plexus papilloma|Juvenile polyposis syndrome|Familial adenomatous polyposis	Testosterone (JAN/USP)|Danazol (JP16/USP/INN)|Flutamide (JP16/USP/INN)|Sirolimus (USAN/INN)|Bicalutamide (JAN/USP/INN)|Nilutamide (USAN/INN)|Metenolone enanthate (JP16)|Imatinib mesilate (JAN)|Gefitinib (JAN/USAN/INN)|Everolimus (JAN/USAN/INN)|Bexarotene (USAN/INN)|Axitinib (JAN/USAN)|Bosutinib (USAN)|Trastuzumab (genetical recombination) (JAN)|Cetuximab (genetical recombination) (JAN)|Dasatinib (INN)|Erlotinib hydrochloride (JAN/USAN)|Lapatinib tosilate hydrate (JAN)|Lestaurtinib (USAN/INN)|Panitumumab (genetical recombination) (JAN)|Pazopanib hydrochloride (JAN/USAN)|Pegaptanib sodium (JAN/USAN)|Semaxanib (USAN/INN)|Tandutinib (USAN/INN)|Temsirolimus (JAN/USAN/INN)|Sorafenib tosilate (JAN)|Vatalanib (USAN/INN)|Sunitinib malate (JAN/USAN)|Vandetanib (JAN/USAN/INN)|Bevacizumab (genetical recombination) (JAN)|Nilotinib hydrochloride hydrate (JAN)|Dasatinib hydrate (JAN)|Erlotinib (INN)|Imatinib (INN)|Lapatinib (INN)|Sorafenib (USAN/INN)|Sunitinib (INN)|Cediranib (USAN/INN)|Cediranib maleate (JAN/USAN)|Neratinib (INN/USAN)|Nilotinib (USAN/INN)|Aflibercept (genetical recombination) (JAN)|Afatinib (USAN/INN)|Afatinib maleate (JAN)|Amuvatinib (USAN/INN)|Amuvatinib hydrochloride (USAN)|Lenvatinib (USAN/INN)|Lenvatinib mesylate (USAN)|Ponatinib (USAN/INN)|Ponatinib hydrochloride (USAN)|Quizartinib (USAN/INN)|Quizartinib dihydrochloride (USAN)|Vismodegib (USAN/INN)|Vemurafenib (USAN/INN)|Zalutumumab (USAN/INN)|Cabozantinib (USAN)|Crenolanib (USAN)|Crenolanib besylate (USAN)|Ganetespib (USAN)|Regorafenib (USAN/INN)|Tivantinib (USAN/INN)	
hsa05217	Basal cell carcinoma - Homo sapiens (human)	Human Diseases; Cancers	7157:TP53|6469:SHH|5727:PTCH1|6608:SMO|27148:STK36|51684:SUFU|2737:GLI3|2736:GLI2|2735:GLI1|650:BMP2|652:BMP4|64399:HHIP|8643:PTCH2|7471:WNT1|7482:WNT2B|7472:WNT2|7473:WNT3|89780:WNT3A|54361:WNT4|7474:WNT5A|81029:WNT5B|7475:WNT6|7477:WNT7B|7476:WNT7A|7479:WNT8B|7478:WNT8A|7483:WNT9A|7484:WNT9B|7480:WNT10B|80326:WNT10A|7481:WNT11|51384:WNT16|8321:FZD1|8324:FZD7|2535:FZD2|7976:FZD3|8322:FZD4|8325:FZD8|7855:FZD5|8323:FZD6|8326:FZD9|11211:FZD10|1856:DVL2|1857:DVL3|1855:DVL1|2932:GSK3B|8312:AXIN1|8313:AXIN2|10297:APC2|324:APC|1499:CTNNB1|6932:TCF7|83439:TCF7L1|6934:TCF7L2|51176:LEF1	Basal cell carcinoma|Basal cell nevus syndrome		Cancer of the skin is the most common cancer in Caucasians and basal cell carcinomas (BCC) account for 90% of all skin cancers. The vast majority of BCC cases are sporadic, though there is a rare familial syndrome basal cell nevus syndrome (BCNS, or Gorlin syndrome) that predisposes to development of BCC. In addition, there is strong epidemiological and genetic evidence that demonstrates UV exposure as a risk factor of prime importance. The development of basal cell carcinoma is associated with constitutive activation of sonic hedgehog signaling. The mutations in SMOH, PTCH1, and SHH in BCCs result in continuous activation of target genes. At a cellular level, sonic hedgehog signaling promotes cell proliferation. Mutations in TP53 are also found with high frequency (>50%) in sporadic BCC.
hsa04950	Maturity onset diabetes of the young - Homo sapiens (human)	Human Diseases; Endocrine and Metabolic Diseases	3087:HHEX|3110:MNX1|3175:ONECUT1|3651:PDX1|2494:NR5A2|50674:NEUROG3|4821:NKX2-2|4825:NKX6-1|5080:PAX6|5078:PAX4|4760:NEUROD1|3280:HES1|6928:HNF1B|3170:FOXA2|389692:MAFA|3172:HNF4A|6927:HNF1A|3174:HNF4G|3171:FOXA3|5313:PKLR|6514:SLC2A2|3630:INS|3375:IAPP|2645:GCK|168620:BHLHA15	Maturity onset diabetes of the young (MODY)|Permanent neonatal diabetes mellitus (PNDM)|Pancreatic agenesis		About 2-5% of type II diabetic patients suffer from a monogenic disease with autosomal dominant inheritance. This monogenic form of type II diabetes is called maturity onset diabetes of the young (MODY).|We now know that MODY is caused by heterozygous mutations in at least five genes encoding transcription factors: HNF4alpha (MODY1), HNF1alpha (MODY3), PDX1 (MODY4), HNF1beta (MODY5) and NEUROD1 (MODY6). MODY2, which is so far the only subtype not related to a transcription factor, is caused by mutations in the glucokinase gene. Mutations of MODY transcription factor genes lead to abnormal expression of genes involved in pancreatic islet development and metabolism.
hsa00531	Glycosaminoglycan degradation - Homo sapiens (human)	Metabolism; Glycan Biosynthesis and Metabolism	3423:IDS|3425:IDUA|411:ARSB|6677:SPAM1|8692:HYAL2|23553:HYAL4|8372:HYAL3|3373:HYAL1|2990:GUSB|10855:HPSE|60495:HPSE2|6448:SGSH|138050:HGSNAT|4669:NAGLU|2588:GALNS|2720:GLB1|2799:GNS|3073:HEXA|3074:HEXB	Mucopolysaccharidosis type IV (MPS4)|GM2 gangliosidoses|Mucopolysaccharidosis type I (MPS1)|Mucopolysaccharidosis type II (MPS2)|Mucopolysaccharidosis type III (MPS3)|Mucopolysaccharidosis type VI (MPS6)|Mucopolysaccharidosis type VII (MPS7)|Mucopolysaccharidosis type IX (MPS9)|GM1 gangliosidosis|Urofacial syndrome		
hsa00190	Oxidative phosphorylation - Homo sapiens (human)	Metabolism; Energy Metabolism	4535:ND1|4536:ND2|4537:ND3|4538:ND4|4539:ND4L|4540:ND5|4541:ND6|4719:NDUFS1|4720:NDUFS2|4722:NDUFS3|4724:NDUFS4|4725:NDUFS5|4726:NDUFS6|374291:NDUFS7|4728:NDUFS8|4723:NDUFV1|4729:NDUFV2|4731:NDUFV3|4694:NDUFA1|4695:NDUFA2|4696:NDUFA3|4697:NDUFA4|56901:NDUFA4L2|4698:NDUFA5|4700:NDUFA6|4701:NDUFA7|4702:NDUFA8|4704:NDUFA9|4705:NDUFA10|4706:NDUFAB1|126328:NDUFA11|55967:NDUFA12|51079:NDUFA13|4707:NDUFB1|4708:NDUFB2|4709:NDUFB3|4710:NDUFB4|4711:NDUFB5|4712:NDUFB6|4713:NDUFB7|4714:NDUFB8|4715:NDUFB9|4716:NDUFB10|54539:NDUFB11|4717:NDUFC1|4718:NDUFC2|6391:SDHC|6392:SDHD|6389:SDHA|6390:SDHB|7386:UQCRFS1|4519:CYTB|1537:CYC1|7384:UQCRC1|7385:UQCRC2|7388:UQCRH|440567:UQCRHL|7381:UQCRB|27089:UQCRQ|29796:UQCR10|10975:UQCR11|1352:COX10|4514:COX3|4512:COX1|4513:COX2|1327:COX4I1|84701:COX4I2|9377:COX5A|1329:COX5B|1337:COX6A1|1339:COX6A2|1340:COX6B1|125965:COX6B2|1345:COX6C|1347:COX7A2|1346:COX7A1|9167:COX7A2L|1349:COX7B|170712:COX7B2|1350:COX7C|1351:COX8A|341947:COX8C|1353:COX11|1355:COX15|10063:COX17|514:ATP5E|513:ATP5D|506:ATP5B|509:ATP5C1|498:ATP5A1|539:ATP5O|4509:ATP8|518:ATP5G3|516:ATP5G1|517:ATP5G2|4508:ATP6|515:ATP5F1|521:ATP5I|522:ATP5J|9551:ATP5J2|10476:ATP5H|10632:ATP5L|9114:ATP6V0D1|245972:ATP6V0D2|9296:ATP6V1F|528:ATP6V1C1|245973:ATP6V1C2|523:ATP6V1A|526:ATP6V1B2|525:ATP6V1B1|529:ATP6V1E1|90423:ATP6V1E2|527:ATP6V0C|533:ATP6V0B|535:ATP6V0A1|50617:ATP6V0A4|23545:ATP6V0A2|10312:TCIRG1|51382:ATP6V1D|8992:ATP6V0E1|155066:ATP6V0E2|9550:ATP6V1G1|534:ATP6V1G2|127124:ATP6V1G3|51606:ATP6V1H|537:ATP6AP1|495:ATP4A|496:ATP4B|479:ATP12A|5464:PPA1|27068:PPA2|64077:LHPP|100532726:NDUFC2-KCTD14	Leber optic atrophy|Mitochondrial respiratory chain deficiencies (MRCD)|Exocrine pancreatic insufficiency, dyserythropoietic anemia, and calvarial hyperostosis|Infantile bilateral striatal necrosis (IBSN)	Lansoprazole (JAN/USP/INN)|Omeprazole (JP16/USP/INN)|Sodium rabeprazole (JP16)|Omeprazole sodium (USAN)|Tenatoprazole (JAN/INN)|Esomeprazole magnesium hydrate (JAN)|Pantoprazole Sodium Hydrate (JAN)|Esomeprazole sodium (USAN)|Omeprazole magnesium (USAN)|Omeprazole sodium injection (JAN)|Pantoprazole (USAN/INN)|Timoprazole (INN)|Picoprazole (INN)|Leminoprazole (INN)|Esomeprazole (INN)|Rabeprazole (INN)|Dexlansoprazole (INN/USAN)|Esomeprazole potassium (USAN)	
hsa00350	Tyrosine metabolism - Homo sapiens (human)	Metabolism; Amino Acid Metabolism	2805:GOT1|2806:GOT2|6898:TAT|259307:IL4I1|3242:HPD|3081:HGD|2954:GSTZ1|2184:FAH|7299:TYR|7054:TH|1638:DCT|7306:TYRP1|1644:DDC|1621:DBH|5409:PNMT|1312:COMT|4129:MAOB|4128:MAOA|314:AOC2|8639:AOC3|222:ALDH3B2|220:ALDH1A3|221:ALDH3B1|218:ALDH3A1|126:ADH1C|131:ADH7|124:ADH1A|125:ADH1B|127:ADH4|128:ADH5|130:ADH6|7173:TPO|51409:HEMK1|131965:METTL6|55798:METTL2B|114049:WBSCR22|316:AOX1|4282:MIF	Alkaptonuria|Tyrosinemia|Oculocutaneous albinism (OCA)|Thyroid dyshormonogenesis|Brunner syndrome|Primary torsion dystonia (PTD)|Dopamine beta-hydroxylase deficiency|Aromatic L-amino acid decarboxylase (AADC) deficiency	Phloroglucinol (JAN)|Isoniazid (JP16/USP/INN)|Thiamazole (JP16/INN)|Methyldopa hydrate (JP16)|Phenelzine sulfate (USP)|Carbidopa hydrate (JP16)|Propylthiouracil (JP16/USP/INN)|Fomepizole (USAN/INN)|Metyrosine (USP)|Entacapone (JAN/USAN/INN)|Selegiline hydrochloride (JAN/USP)|Tolcapone (JAN/USAN/INN)|Tranylcypromine sulfate (USP XXI)|Lazabemide hydrochloride (JAN/USAN)|Flopropione (JP16/INN)|Amezinium metilsulfate (JAN)|Isoniazid calcium pyruvinate (JAN)|Benserazide hydrochloride (JP16)|Safrazine hydrochloride (JAN)|Isoniazid sodium methanesulfonate hydrate (JAN)|Toloxatone (INN)|Brofaromine (INN)|Moclobemide (USAN/INN)|Rasagiline mesylate (USAN)|Befloxatone (INN)|Pargyline hydrochloride (USAN)|Iproniazid (INN)|Isocarboxazid (INN)|Cimoxatone (INN)|Benserazide (USAN/INN)|Ladostigil tartrate (USAN)|Nitecapone (INN)|Clorgiline (INN)|Caroxazone (USAN/INN)|Selegiline (USAN/INN)|Mofegiline hydrochloride (USAN)|Lazabemide (USAN/INN)|Milacemide hydrochloride (USAN)|Nitisinone (JAN/USAN/INN)|Methylthiouracil (INN)|Nialamide (INN)|Iproclozide (INN)|Benzylthiouracil|Iproniazid phosphate|Methyldopa (INN)|Phenelzine (BAN)|Polyphloroglucinol phosphate|Pargyline (INN)|Rasagiline (USAN/INN)|Tranylcypromine (INN)	
hsa04728	Dopaminergic synapse - Homo sapiens (human)	Organismal Systems; Nervous System	7054:TH|1644:DDC|6571:SLC18A2|6570:SLC18A1|1812:DRD1|1816:DRD5|50632:CALY|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|3708:ITPR1|3709:ITPR2|3710:ITPR3|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5579:PRKCB|5578:PRKCA|5582:PRKCG|2353:FOS|2778:GNAS|2774:GNAL|111:ADCY5|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|1385:CREB1|1386:ATF2|468:ATF4|10488:CREB3|64764:CREB3L2|84699:CREB3L3|148327:CREB3L4|90993:CREB3L1|9586:CREB5|1388:ATF6B|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|5602:MAPK10|5601:MAPK9|5599:MAPK8|84152:PPP1R1B|5501:PPP1CC|5499:PPP1CA|5500:PPP1CB|6323:SCN1A|775:CACNA1C|776:CACNA1D|773:CACNA1A|774:CACNA1B|3760:KCNJ3|3763:KCNJ6|3765:KCNJ9|3762:KCNJ5|1814:DRD3|1815:DRD4|2773:GNAI3|2770:GNAI1|2771:GNAI2|2775:GNAO1|2782:GNB1|2783:GNB2|2784:GNB3|59345:GNB4|10681:GNB5|54331:GNG2|2785:GNG3|2786:GNG4|2787:GNG5|2788:GNG7|94235:GNG8|2790:GNG10|2791:GNG11|55970:GNG12|51764:GNG13|2792:GNGT1|2793:GNGT2|1813:DRD2|5516:PPP2CB|5515:PPP2CA|5518:PPP2R1A|5519:PPP2R1B|55844:PPP2R2D|5520:PPP2R2A|5522:PPP2R2C|5521:PPP2R2B|5523:PPP2R3A|28227:PPP2R3B|55012:PPP2R3C|5525:PPP2R5A|5528:PPP2R5D|5526:PPP2R5B|5527:PPP2R5C|5529:PPP2R5E|207:AKT1|208:AKT2|10000:AKT3|2931:GSK3A|2932:GSK3B|2903:GRIN2A|2904:GRIN2B|2890:GRIA1|2891:GRIA2|2892:GRIA3|2893:GRIA4|3800:KIF5C|3798:KIF5A|3799:KIF5B|9575:CLOCK|406:ARNTL|6531:SLC6A3|4129:MAOB|4128:MAOA|1312:COMT|409:ARRB2	Brunner syndrome|Syndromic X-linked mental retardation with epilepsy or seizures|Episodic ataxias|Familial or sporadic hemiplegic migraine|Febrile seizures|Primary torsion dystonia (PTD)|Aromatic L-amino acid decarboxylase (AADC) deficiency	Levodopa (JP16/USP/INN)|Cocaine (USP)|Phloroglucinol (JAN)|Reserpine (JP16/USP/INN)|Chlorpromazine (USP/INN)|Clozapine (JAN/USP/INN)|Disopyramide (JP16/USAN/INN)|Isoniazid (JP16/USP/INN)|Mazindol (JAN/USP/INN)|Levomepromazine (USAN/INN)|Pergolide mesilate (JAN)|Phenelzine sulfate (USP)|Zonisamide (JAN/USAN/INN)|Carbidopa hydrate (JP16)|Pramipexole hydrochloride hydrate (JAN)|Amantadine hydrochloride (JP16/USP)|Bromocriptine mesilate (JP16)|Entacapone (JAN/USAN/INN)|Selegiline hydrochloride (JAN/USP)|Tolcapone (JAN/USAN/INN)|Chlorpromazine hydrochloride (JP16/USP)|Tranylcypromine sulfate (USP XXI)|Cabergoline (JAN/USAN/INN)|Lazabemide hydrochloride (JAN/USAN)|Ergometrine maleate (JP16)|Flopropione (JP16/INN)|Amezinium metilsulfate (JAN)|Talipexole hydrochloride (JAN)|Tiapride hydrochloride (JP16)|Safrazine hydrochloride (JAN)|Ziprasidone hydrochloride hydrate (JAN)|Amphetamine sulfate (USP)|Dextroamphetamine sulfate (USP)|Ziprasidone mesylate (USAN)|Methamphetamine hydrochloride (JP16/USP)|Toloxatone (INN)|Brofaromine (INN)|Moclobemide (USAN/INN)|Rasagiline mesylate (USAN)|Befloxatone (INN)|Pargyline hydrochloride (USAN)|Sibutramine hydrochloride hydrate (JAN)|Iproniazid (INN)|Isocarboxazid (INN)|Cimoxatone (INN)|Ladostigil tartrate (USAN)|Clorgiline (INN)|Chlorpromazine hibenzate (JAN)|Caroxazone (USAN/INN)|Selegiline (USAN/INN)|Chlorpromazine phenolphthalinate (JAN)|Lazabemide (USAN/INN)|Lergotrile (USAN/INN)|Lergotrile mesylate (USAN)|Lurasidone hydrochloride (JAN/USAN)|Milacemide hydrochloride (USAN)|Minaprine (USAN/INN)|Minaprine hydrochloride (USAN)|Ziconotide (USAN/INN)|Nialamide (INN)|Iproclozide (INN)|Iproniazid phosphate|Metamfetamine (INN)|Phenelzine (BAN)|Pargyline (INN)|Rasagiline (USAN/INN)|Sibutramine (INN)|Tetrabenazine (JAN/INN)|Tranylcypromine (INN)|Ziconotide acetate	Dopamine (DA) is  an important and prototypical slow neurotransmitter in the mammalian brain, where it controls a variety of functions including locomotor activity, motivation and reward, learning and memory, and endocrine regulation. Once released from presynaptic axonal terminals, DA interacts with at least five receptor subtypes in the central nervous system (CNS), which have been divided into two groups: the D1-like receptors (D1Rs), comprising D1 and D5 receptors, both positively coupled to adenylyl cyclase and cAMP production, and the D2-like receptors (D2Rs), comprising D2, D3, and D4 receptors, whose activation results in inhibition of adenylyl cyclase and suppression of cAMP production. In addition, D1Rs and D2Rs modulate intracellular Ca2+ levels and a number of Ca2+ -dependent intracellular signaling processes. Through diverse cAMP- and Ca2+-dependent and - independent mechanisms, DA influences neuronal activity, synaptic plasticity, and behavior. Presynaptically localized D2Rs regulate synthesis and release of DA as the main autoreceptor of the dopaminergic system.
hsa04930	Type II diabetes mellitus - Homo sapiens (human)	Human Diseases; Endocrine and Metabolic Diseases	3630:INS|3643:INSR|8471:IRS4|8660:IRS2|3667:IRS1|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|6517:SLC2A4|9370:ADIPOQ|5594:MAPK1|5595:MAPK3|2475:MTOR|8651:SOCS1|8835:SOCS2|9021:SOCS3|122809:SOCS4|3551:IKBKB|5602:MAPK10|5601:MAPK9|5599:MAPK8|7124:TNF|3651:PDX1|389692:MAFA|6514:SLC2A2|3101:HK3|3099:HK2|3098:HK1|80201:HKDC1|2645:GCK|5315:PKM2|5313:PKLR|3767:KCNJ11|6833:ABCC8|775:CACNA1C|776:CACNA1D|773:CACNA1A|774:CACNA1B|777:CACNA1E|8913:CACNA1G|5580:PRKCD|5581:PRKCE|5590:PRKCZ	Type II diabetes mellitus|Maturity onset diabetes of the young (MODY)|Permanent neonatal diabetes mellitus (PNDM)|Transient neonatal diabetes mellitus (TNDM)|Leprechaunism |Pancreatic agenesis|Rabson-Mendenhall syndrome|Adiponectin deficiency	Insulin (JAN/USP)|Acetohexamide (JP16/USP/INN)|Chlorpropamide (JP16/USP/INN)|Diazoxide (JAN/USP/INN)|Glipizide (USP/INN)|Glibenclamide (JP16/INN)|Tolazamide (JP16/USP/INN)|Tolbutamide (JP16/USP/INN)|Glimepiride (JP16/USP/INN)|Repaglinide (JAN/USP/INN)|Nateglinide (JP16/USAN/INN)|Glymidine sodium (JAN/USAN/INN)|Gliclazide (JP16/INN)|Glyclopyramide (JAN/INN)|Mitiglinide calcium hydrate (JAN)|Carbutamide (INN)|Glibornuride (USAN/INN)|Gliquidone (INN)|Insulin human (genetical recombination) (JP16)|Insulin glargine (genetical recombination) (JAN)|Insulin aspart (genetical recombination) (JAN)|Insulin lispro (genetical recombination) (JAN)|Insulin detemir (genetical recombination) (JAN)|Insulin glulisine (genetical recombination) (JAN)|Insulin human, isophane (USP)|Insulin human zinc (USP)|Insulin human zinc, extended (USP)|Insulin I 125 (USAN)|Insulin I 131 (USAN)|Insulin, dalanated (USAN)|Isophane insulin injection (aqueous suspension) (JAN)|Insulin, neutral (USAN)|Insulin zinc, extended (USP)|Insulin zinc, prompt (USP)|Insulin zinc (USP)|Proinsulin human (USAN)|Tolbutamide sodium, sterile|Metahexamide (INN)|Glisoxepide (INN)|Insulin injection, biphasic isophane (BAN)|Insulin degludec (genetical recombination) (JAN)	Insulin resistance is strongly associated with type II diabetes. "Diabetogenic" factors including FFA, TNFalpha and cellular stress induce insulin resistance through inhibition of IRS1 functions. Serine/threonine phosphorylation, interaction with SOCS, regulation of the expression, modification of the cellular localization, and degradation represent the molecular mechanisms stimulated by them. Various kinases (ERK, JNK, IKKbeta, PKCzeta, PKCtheta and mTOR) are involved in this process.|The development of type II diabetes requires impaired beta-cell function. Chronic hyperglycemia has been shown to induce multiple defects in beta-cells. Hyperglycemia has been proposed to lead to large amounts of reactive oxygen species (ROS) in beta-cells, with subsequent damage to cellular components including PDX-1. Loss of PDX-1, a critical regulator of insulin promoter activity, has also been proposed as an important mechanism leading to beta-cell dysfunction.|Although there is little doubt as to the importance of genetic factors in type II diabetes, genetic analysis is difficult due to complex interaction among multiple susceptibility genes and between genetic and environmental factors. Genetic studies have therefore given very diverse results. Kir6.2 and IRS are two of the candidate genes. It is known that Kir6.2 and IRS play central roles in insulin secretion and insulin signal transmission, respectively.
hsa04650	Natural killer cell mediated cytotoxicity - Homo sapiens (human)	Organismal Systems; Immune System	3133:HLA-E|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|3812:KIR3DL2|3811:KIR3DL1|3805:KIR2DL4|3803:KIR2DL2|57292:KIR2DL5A|3802:KIR2DL1|3804:KIR2DL3|3822:KLRC2|3823:KLRC3|3821:KLRC1|3824:KLRD1|5777:PTPN6|5781:PTPN11|3383:ICAM1|3384:ICAM2|3683:ITGAL|3689:ITGB2|2185:PTK2B|10451:VAV3|7409:VAV1|7410:VAV2|5879:RAC1|5880:RAC2|5881:RAC3|5058:PAK1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|7124:TNF|1437:CSF2|3458:IFNG|3806:KIR2DS1|3810:KIR2DS5|3809:KIR2DS4|3808:KIR2DS3|9436:NCR2|7305:TYROBP|3932:LCK|100132941:uncharacterized|100291917:uncharacterized|2215:FCGR3B|2214:FCGR3A|9437:NCR1|259197:NCR3|2207:FCER1G|919:CD247|7535:ZAP70|6850:SYK|3937:LCP2|27040:LAT|5335:PLCG1|5336:PLCG2|6452:SH3BP2|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|2534:FYN|25759:SHC2|6464:SHC1|53358:SHC3|399694:SHC4|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|369:ARAF|673:BRAF|5894:RAF1|100507436:MICA|4277:MICB|79465:ULBP3|80329:ULBP1|80328:ULBP2|135250:RAET1E|154064:RAET1L|353091:RAET1G|22914:KLRK1|10870:HCST|962:CD48|51744:CD244|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|4776:NFATC4|4772:NFATC1|4773:NFATC2|4775:NFATC3|10725:NFAT5|5579:PRKCB|5578:PRKCA|5582:PRKCG|117157:SH2D1B|4068:SH2D1A|3459:IFNGR1|3460:IFNGR2|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3456:IFNB1|3454:IFNAR1|3455:IFNAR2|8743:TNFSF10|8793:TNFRSF10D|8794:TNFRSF10C|8795:TNFRSF10B|8797:TNFRSF10A|356:FASLG|355:FAS|3002:GZMB|5551:PRF1|836:CASP3|637:BID	NK cell defects|Leprosy|Metachondromatosis	Interferon alfa-2a (genetical recombination) (JAN)|Interferon beta-1b (genetical recombination) (JAN)|Interferon gamma-1b (USAN/INN)|Adalimumab (genetical recombination) (JAN)|Interferon alfacon-1 (genetical recombination) (JAN)|Interferon alfa-2b (genetical recombination) (JAN)|Peginterferon alfa-2a (genetical recombination) (JAN)|Peginterferon alfa-2b (generical recombination) (JAN)|Alicaforsen sodium (USAN)|Interferon beta (JAN)|Interferon alfa (BALL-1) (JAN)|Interferon gamma-1a (genetical recombination) (JAN)|Certolizumab pegol (genetical recombination) (JAN)|Efalizumab (USAN/INN)|Interferon alfa-n1 (USAN)|Interferon beta-1a (genetical recombination) (JAN)|Omalizumab (genetical recombination) (JAN)|Sorafenib tosilate (JAN)|Sorafenib (USAN/INN)|Interferon gamma-n1 (JAN)|Albinterferon alfa-2b (USAN)|Blinatumomab (USAN/INN)	Natural killer (NK) cells are lymphocytes of the innate immune system that are involved in early defenses against both allogeneic (nonself) cells and autologous cells undergoing various forms of stress, such as infection with viruses, bacteria, or parasites or malignant transformation. Although NK cells do not express classical antigen receptors of the immunoglobulin gene family, such as the antibodies produced by B cells or the T cell receptor expressed by T cells, they are equipped with various receptors whose engagement allows them to discriminate between target and nontarget cells. Activating receptors bind ligands on the target cell surface and trigger NK cell activation and target cell lysis. However Inhibitory receptors recognize MHC class I molecules (HLA) and inhibit killing by NK cells by overruling the actions of the activating receptors. This inhibitory signal is lost when the target cells do not express MHC class I and perhaps also in cells infected with virus, which might inhibit MHC class I exprssion or alter its conformation. The mechanism of NK cell killing is the same as that used by the cytotoxic T cells generated in an adaptive immune response; cytotoxic granules are released onto the surface of the bound target cell, and the effector proteins they contain penetrate the cell membrane and induce programmed cell death.
hsa00140	Steroid hormone biosynthesis - Homo sapiens (human)	Metabolism; Lipid Metabolism	1583:CYP11A1|1586:CYP17A1|412:STS|6820:SULT2B1|1589:CYP21A2|3283:HSD3B1|3284:HSD3B2|1109:AKR1C4|8644:AKR1C3|1646:AKR1C2|1645:AKR1C1|1584:CYP11B1|1585:CYP11B2|6718:AKR1D1|3290:HSD11B1|3291:HSD11B2|9420:CYP7B1|6783:SULT1E1|3292:HSD17B1|51144:HSD17B12|3294:HSD17B2|8630:HSD17B6|51478:HSD17B7|7923:HSD17B8|1543:CYP1A1|1551:CYP3A7|1577:CYP3A5|64816:CYP3A43|1576:CYP3A4|1545:CYP1B1|1588:CYP19A1|1581:CYP7A1|7363:UGT2B4|574537:UGT2A2|7367:UGT2B17|7365:UGT2B10|7364:UGT2B7|7366:UGT2B15|54577:UGT1A7|10720:UGT2B11|54490:UGT2B28|54579:UGT1A5|54659:UGT1A3|54657:UGT1A4|54578:UGT1A6|54576:UGT1A8|54600:UGT1A9|10941:UGT2A1|54575:UGT1A10|79799:UGT2A3|54658:UGT1A1|6715:SRD5A1|6716:SRD5A2|79644:SRD5A3|1312:COMT|3293:HSD17B3	X-linked ichthyosis (XLI)|Congenital adrenal hyperplasia (CAH)|Aldosterone synthase deficiency|Apparent mineralocorticoid excess syndrome|46,XX disorders of sex development (Disorders related to androgen excess)|Glucocorticoid-remediable aldosteronism (GRA)|46,XY disorders of sex development (Disorders in androgen synthesis or action)|Congenital bile acid synthesis defect (CBAS)|Aromatase excess syndrome|Peters anomaly|Cortisone reductase deficiency (CRD)|Primary congenital glaucoma (PCG)	Phloroglucinol (JAN)|Testolactone (USP/INN)|Glycyrrhetinic acid (JAN)|Finasteride (JAN/USP/INN)|Metyrapone (JP16/USP/INN)|Mitotane (JAN/USP/INN)|Aminoglutethimide (USP/INN)|Entacapone (JAN/USAN/INN)|Tolcapone (JAN/USAN/INN)|Anastrozole (JAN/USAN/INN)|Exemestane (JAN/USP/INN)|Letrozole (JAN/USP/INN)|Flopropione (JP16/INN)|Carbenoxolone sodium (JAN/USAN)|Fadrozole hydrochloride (USAN)|Bexlosteride (USAN/INN)|Nitecapone (INN)|Plomestane (USAN/INN)|Fadrozole hydrochloride hydrate (JAN)|Liarozole fumarate (USAN)|Liarozole hydrochloride (USAN)|Vorozole (USAN/INN)|Dutasteride (JAN/USAN/INN)|Idronoxil (USAN/INN)|Metyrapone tartrate (USAN)|Carbenoxolone (INN)|Fadrozole (INN)|Polyphloroglucinol phosphate	Steroid hormones derived from cholesterol are a class of biologically active compounds in vertebrates. The cholesterol side-chain cleavage enzyme CYP11A1 catalyzes conversion of cholesterol, a C27 compound, to the first C21 steroid, pregnenolone, which is converted by a bifunctional enzyme complex to the gestagen hormone, progesterone [MD:M00107]. Pregnenolone and progesterone are the starting materials for the three groups of steroids: C21 steroids of glucocorticoids and mineralocorticoids, C19 steroids of androgens, and C18 steroids of estrogens. (i) Progesterone is converted by hydroxylations at carbons 21 and 11 to corticosterone, which is further modified by hydroxylation and oxydoreduction at carbon 18 to yield aldosterone, a mineralcorticoid [MD:M00108]. Cortisol, the main glucocorticoid, is formed from 17alpha-hydroxyprogesterone with 11-deoxycortisol as an intermediate [MD:M00109]. (ii) Male hormone testosterone is formed from pregnenolone by two pathways, delta5 pathway via dehydroepiandrosterone and delta4 pathway via androstenedione [MD:M00110]. The enzyme CYP17A1 is responsible for the 17,20 lyase and 17alpha-hydroxylase activities in respective pathways. (iii) Female hormones estrone and estradiol are formed from testosterone and 4-androstene-3,17-dione by oxidative removal of the C19 methyl group and subsequent aromatization of ring A [MD:M00111]. In addition to these three groups, recent studies show that there is another group, termed neurosteroids, synthesized in the brain rather than the peripheral endocrine gland.
hsa04260	Cardiac muscle contraction - Homo sapiens (human)	Organismal Systems; Circulatory System	775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|782:CACNB1|783:CACNB2|784:CACNB3|785:CACNB4|781:CACNA2D1|9254:CACNA2D2|55799:CACNA2D3|93589:CACNA2D4|786:CACNG1|10369:CACNG2|10368:CACNG3|27092:CACNG4|27091:CACNG5|59285:CACNG6|59284:CACNG7|59283:CACNG8|6262:RYR2|7134:TNNC1|7137:TNNI3|7139:TNNT2|7168:TPM1|7169:TPM2|7170:TPM3|7171:TPM4|70:ACTC1|4634:MYL3|4633:MYL2|7386:UQCRFS1|4519:CYTB|1537:CYC1|7384:UQCRC1|7385:UQCRC2|7388:UQCRH|440567:UQCRHL|7381:UQCRB|27089:UQCRQ|29796:UQCR10|10975:UQCR11|4514:COX3|4512:COX1|4513:COX2|1327:COX4I1|84701:COX4I2|9377:COX5A|1329:COX5B|1337:COX6A1|1339:COX6A2|1340:COX6B1|125965:COX6B2|1345:COX6C|1347:COX7A2|1346:COX7A1|9167:COX7A2L|1349:COX7B|170712:COX7B2|1350:COX7C|1351:COX8A|341947:COX8C|476:ATP1A1|480:ATP1A4|478:ATP1A3|477:ATP1A2|481:ATP1B1|482:ATP1B2|483:ATP1B3|23439:ATP1B4|486:FXYD2|6548:SLC9A1|10479:SLC9A6|4624:MYH6|4625:MYH7|488:ATP2A2|6546:SLC8A1	Distal muscular dystrophies|Scapuloperoneal myopathy (SPM)|Nemaline myopathy|Congenital fiber type disproportion (CFTD)|Cap myopathy|Myosin storage myopathy (MSM)|Brugada syndrome (BRS)|Hypokalemic periodic paralysis (HypoPP)|Episodic ataxias|Familial or sporadic hemiplegic migraine|Idiopathic generalied epilepsies (IGEs)|Distal arthrogryposis (DA)|Primary torsion dystonia (PTD)|Catecholaminergic polymorphic ventricular tachycardia	Digitoxin (JP16/USP/INN)|Digoxin (JP16/USP)|Felodipine (JAN/USP/INN)|Isradipine (USP/INN)|Nifedipine (JP16/USP/INN)|Nimodipine (USAN/INN)|Amlodipine besilate (JP16)|Diltiazem hydrochloride (JP16/USP)|Nicardipine hydrochloride (JP16/USAN)|Nisoldipine (JAN/USAN/INN)|Verapamil hydrochloride (JP16/USP)|Nitrendipine (JP16/USAN/INN)|Bepridil hydrochloride hydrate (JAN)|Barnidipine hydrochloride (JAN)|Azelnidipine (JAN/INN)|Cilnidipine (JAN/INN)|Deslanoside (JP16/USP/INN)|Proscillaridin (JAN/USAN/INN)|Manidipine hydrochloride (JP16)|Aranidipine (JAN/INN)|Efonidipine hydrochloride ethanolate (JAN)|Nilvadipine (JP16/USAN/INN)|Gallopamil hydrochloride (JAN)|Lanatoside C (JP16/INN)|Benidipine hydrochloride (JP16)|Verapamil (USAN/INN)|Dronedarone (INN)|Metildigoxin (JP16)|Amlodipine maleate (USAN)|Darodipine (USAN/INN)|Diltiazem malate (USAN)|Dronedarone hydrochloride (USAN)|Lacidipine (USAN/INN)|Acetyldigitoxin (INN)|Gitoformate (INN)|Amlodipine (INN)|Barnidipine (INN)|Benidipine (INN)|Bepridil (INN)|Acetyldigoxin|Diltiazem (INN)|Efonidipine (INN)|Gallopamil (INN)|Manidipine (INN)|Nicardipine (INN)	Contraction of the heart is a complex process initiated by the electrical excitation of cardiac myocytes (excitation-contraction coupling, ECC). In cardiac myocytes, Ca2+ influx induced by activation of voltage-dependent L-type Ca channels (DHP receptors) upon membrane depolarization triggers the release of Ca2+ via Ca2+ release channels (ryanodine receptors) of sarcoplasmic reticulum (SR) through a Ca2+ -induced Ca release (CICR) mechanism. Ca2+ ions released via the CICR mechanism diffuse through the cytosolic space to contractile proteins to bind to troponinC resulting in the release of inhibition induced by troponinI. The Ca2+ binding to troponinC thereby triggers the sliding of thin and thick filaments, that is, the activation of a crossbridge and subsequent cardiac force development and/or cell shortening. Recovery occurs as Ca2+ is pumped out of the cell by the Na+/Ca2+ exchanger (NCX) or is returned to the sarcoplasmic reticulum (SR) by sarco(endo)plasmic Ca2+ -ATPase (SERCA) pumps on the non-junctional region of the SR.
hsa00053	Ascorbate and aldarate metabolism - Homo sapiens (human)	Metabolism; Carbohydrate Metabolism	7358:UGDH|7363:UGT2B4|574537:UGT2A2|7367:UGT2B17|7365:UGT2B10|7364:UGT2B7|7366:UGT2B15|54577:UGT1A7|10720:UGT2B11|54490:UGT2B28|54579:UGT1A5|54659:UGT1A3|54657:UGT1A4|54578:UGT1A6|54576:UGT1A8|54600:UGT1A9|10941:UGT2A1|54575:UGT1A10|79799:UGT2A3|54658:UGT1A1|55586:MIOX|9104:RGN|219:ALDH1B1|224:ALDH3A2|217:ALDH2|501:ALDH7A1|223:ALDH9A1		Cyanamide (JP16)|Disulfiram (JP16/USP/INN)	
hsa04145	Phagosome - Homo sapiens (human)	Cellular Processes; Transport and Catabolism	9341:VAMP3|23673:STX12|8417:STX7|60:ACTB|71:ACTG1|11151:CORO1A|53407:STX18|9554:SEC22B|3133:HLA-E|3134:HLA-F|3107:HLA-C|3106:HLA-B|3105:HLA-A|3135:HLA-G|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|5868:RAB5A|5869:RAB5B|5878:RAB5C|8411:EEA1|5289:PIK3C3|7037:TFRC|9146:HGS|523:ATP6V1A|526:ATP6V1B2|525:ATP6V1B1|528:ATP6V1C1|245973:ATP6V1C2|51382:ATP6V1D|529:ATP6V1E1|90423:ATP6V1E2|9296:ATP6V1F|9550:ATP6V1G1|534:ATP6V1G2|127124:ATP6V1G3|8992:ATP6V0E1|155066:ATP6V0E2|535:ATP6V0A1|50617:ATP6V0A4|23545:ATP6V0A2|10312:TCIRG1|9114:ATP6V0D1|245972:ATP6V0D2|51606:ATP6V1H|527:ATP6V0C|533:ATP6V0B|537:ATP6AP1|7879:RAB7A|338382:RAB7B|83547:RILP|1778:DYNC1H1|79659:DYNC2H1|1780:DYNC1I1|1781:DYNC1I2|1783:DYNC1LI2|51143:DYNC1LI1|112714:TUBA3E|10376:TUBA1B|113457:TUBA3D|7846:TUBA1A|7278:TUBA3C|51807:TUBA8|84790:TUBA1C|79861:TUBAL3|7277:TUBA4A|10383:TUBB4B|10382:TUBB4A|7280:TUBB2A|10381:TUBB3|81027:TUBB1|84617:TUBB6|203068:TUBB|347733:TUBB2B|347688:TUBB8|3920:LAMP2|3916:LAMP1|200576:PIKFYVE|4074:M6PR|4842:NOS1|4353:MPO|1514:CTSL1|1520:CTSS|55176:SEC61A2|29927:SEC61A1|10952:SEC61B|23480:SEC61G|6890:TAP1|6891:TAP2|811:CALR|821:CANX|2204:FCAR|2213:FCGR2B|2209:FCGR1A|9103:FCGR2C|2212:FCGR2A|2215:FCGR3B|2214:FCGR3A|100132941:uncharacterized|100291917:uncharacterized|715:C1R|3684:ITGAM|3689:ITGB2|718:C3|78989:COLEC11|81035:COLEC12|4153:MBL2|653509:SFTPA1|6441:SFTPD|3685:ITGAV|3673:ITGA2|3678:ITGA5|3688:ITGB1|3690:ITGB3|3693:ITGB5|1311:COMP|7059:THBS3|7058:THBS2|7060:THBS4|7057:THBS1|7097:TLR2|10333:TLR6|7099:TLR4|929:CD14|4360:MRC1|9902:MRC2|22925:PLA2R1|10332:CLEC4M|30835:CD209|64581:CLEC7A|4481:MSR1|8685:MARCO|4973:OLR1|949:SCARB1|948:CD36|1535:CYBA|50508:NOX3|1536:CYBB|27035:NOX1|5879:RAC1|653361:NCF1|4688:NCF2|4689:NCF4	Asphyxiating thoracic dystrophy|Macular degeneration|Congenital fibrosis of the extraocular muscles (CFEOM)|Distal hereditary motor neuropathies (dHMN)|Fleck corneal dystrophy (FCD)|Bare lymphocyte syndrome (BLS) type1|CD36 deficiency|Chronic Mucocutaneous Candidiasis (CMC)	Valategrast hydrochloride (USAN)	Phagocytosis is the process of taking in relatively large particles by a cell, and is a central mechanism in the tissue remodeling, inflammation, and defense against infectious agents. A phagosome is formed when the specific receptors on the phagocyte surface recognize ligands on the particle surface. After formation, nascent phagosomes progressively acquire digestive characteristics. This maturation of phagosomes involves regulated interaction with the other membrane organelles, including recycling endosomes, late endosomes and lysosomes. The fusion of phagosomes and lysosomes releases toxic products that kill most bacteria and degrade them into fragments. However, some bacteria have strategies to escape the bactericidal mechanisms associated with phagocytosis and survive within host phagocytes.
hsa05220	Chronic myeloid leukemia - Homo sapiens (human)	Human Diseases; Cancers	613:BCR|25:ABL1|1399:CRKL|1398:CRK|23624:CBLC|868:CBLB|867:CBL|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|207:AKT1|208:AKT2|10000:AKT3|572:BAD|598:BCL2L1|1147:CHUK|3551:IKBKB|8517:IKBKG|4792:NFKBIA|4790:NFKB1|5970:RELA|4193:MDM2|7157:TP53|1027:CDKN1B|2885:GRB2|9846:GAB2|5781:PTPN11|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|5894:RAF1|369:ARAF|673:BRAF|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|25759:SHC2|6464:SHC1|53358:SHC3|399694:SHC4|4609:MYC|6776:STAT5A|6777:STAT5B|1029:CDKN2A|1026:CDKN1A|595:CCND1|1019:CDK4|1021:CDK6|5925:RB1|1871:E2F3|1869:E2F1|1870:E2F2|7040:TGFB1|7042:TGFB2|7043:TGFB3|7046:TGFBR1|7048:TGFBR2|4089:SMAD4|2122:MECOM|861:RUNX1|1488:CTBP2|1487:CTBP1|3066:HDAC2|3065:HDAC1|4088:SMAD3	Chronic myeloid leukemia (CML)	Imatinib mesilate (JAN)|Dasatinib (INN)|Nilotinib hydrochloride hydrate (JAN)|Dasatinib hydrate (JAN)|Imatinib (INN)|Nilotinib (USAN/INN)	Chronic myelogenous leukemia (CML) originates in a pluripotent hematopoetic stem cell of the bone marrow and is characterized by greatly increased numbers of granulocytes in the blood. Myeloid and other hematopoetic cell lineages are involved in the process of clonal proliferation and differentiation. On the cellular level, CML is associated with a specific chromosome abnormality, the t(9; 22) reciprocal translocation that forms the Philadelphia (Ph) chromosome. The Ph chromosome is the result of a molecular rearrangement between the c-ABL proto-oncogene on chromosome 9 and the BCR (breakpoint cluster region) gene on chromosome 22.  The BCR/ABL fusion gene encodes p210 BCR/ABL, an oncoprotein, which, unlike the normal p145 c-Abl, has constitutive tyrosine kinase activity and is predominantly localized in the cytoplasm. While fusion of c-ABL and BCR is believed to be the primary cause of the chronic phase of CML, progression to blast crisis requires other molecular changes. Common secondary abnormalities include mutations in TP53, RB, and p16/INK4A, or overexpression of genes such as EVI1. Additional chromosome translocations are also observed,such as t(3;21)(q26;q22), which generates AML1-EVI1.
hsa05142	Chagas disease (American trypanosomiasis) - Homo sapiens (human)	Human Diseases; Infectious Diseases	7099:TLR4|148022:TICAM1|7097:TLR2|10333:TLR6|54106:TLR9|4615:MYD88|3654:IRAK1|51135:IRAK4|7189:TRAF6|6416:MAP2K4|5602:MAPK10|5601:MAPK9|5599:MAPK8|5594:MAPK1|5595:MAPK3|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|2353:FOS|3725:JUN|8517:IKBKG|1147:CHUK|3551:IKBKB|4792:NFKBIA|4790:NFKB1|5970:RELA|3456:IFNB1|6352:CCL5|6347:CCL2|7124:TNF|3592:IL12A|3593:IL12B|3569:IL6|3576:IL8|6348:CCL3|6349:CCL3L1|414062:CCL3L3|3553:IL1B|5518:PPP2R1A|5519:PPP2R1B|55844:PPP2R2D|5520:PPP2R2A|5522:PPP2R2C|5521:PPP2R2B|5516:PPP2CB|5515:PPP2CA|3458:IFNG|3459:IFNGR1|3460:IFNGR2|7132:TNFRSF1A|4843:NOS2|718:C3|811:CALR|712:C1QA|713:C1QB|714:C1QC|3586:IL10|7040:TGFB1|7042:TGFB2|7043:TGFB3|1636:ACE|624:BDKRB2|2776:GNAQ|2767:GNA11|9630:GNA14|2769:GNA15|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|2773:GNAI3|2770:GNAI1|2771:GNAI2|2775:GNAO1|2778:GNAS|2774:GNAL|107:ADCY1|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|207:AKT1|208:AKT2|10000:AKT3|7048:TGFBR2|7046:TGFBR1|4087:SMAD2|4088:SMAD3|5054:SERPINE1|356:FASLG|355:FAS|8772:FADD|841:CASP8|8837:CFLAR|915:CD3D|916:CD3E|917:CD3G|919:CD247|3558:IL2	Chagas disease		Trypanosoma cruzi is an intracellular protozoan parasite that causes Chagas disease. The parasite life cycle involves hematophagous reduviid bugs as vectors. Once parasites enter the host body, they invade diverse host cells including cardiomyocytes. Establishment of infection depends on various parasite molecules such as cruzipain, oligopeptidase B, and trans-sialidase that activate Ca2+ signaling. Internalized parasites escape from the parasitophorous vacuole using secreted pore-forming TcTOX molecule and replicate in the cytosol. Multiplied parasites eventually lyse infected host cells and are released in the circulation. During these events, the parasites manipulate host innate immunity and elicit cardiomyocyte hypertrophy. T lymphocyte responses are also disturbed.
hsa00970	Aminoacyl-tRNA biosynthesis - Homo sapiens (human)	Genetic Information Processing; Translation	4553:TRNA|4573:TRNR|4570:TRNN|4555:TRND|4511:TRNC|4572:TRNQ|4556:TRNE|4563:TRNG|4564:TRNH|4565:TRNI|4568:TRNL2|4567:TRNL1|4566:TRNK|4569:TRNM|4558:TRNF|4571:TRNP|4575:TRNS2|4574:TRNS1|4576:TRNT|4578:TRNW|4579:TRNY|4577:TRNV|124454:EARS2|2058:EPRS|5859:QARS|57505:AARS2|16:AARS|1615:DARS|55157:DARS2|4677:NARS|79731:NARS2|2617:GARS|6897:TARS|123283:TARSL2|80222:TARS2|54938:SARS2|6301:SARS|118672:PSTK|51091:SEPSECS|833:CARS|79587:CARS2|92935:MARS2|4141:MARS|123263:MTFMT|7407:VARS|57176:VARS2|23395:LARS2|51520:LARS|3376:IARS|55699:IARS2|3735:KARS|5917:RARS|57038:RARS2|25973:PARS2|3035:HARS|23438:HARS2|2193:FARSA|10667:FARS2|10056:FARSB|8565:YARS|51067:YARS2|10352:WARS2|7453:WARS	Charcot-Marie-Tooth disease (CMT)|Progressive myoclonic epilepsy (PME)|Distal hereditary motor neuropathies (dHMN)|Leukoencephalopathy with brain stem and spinal cord involvement and lactate elevation (LBSL)|Pontocerebellar hypoplasia|Myopathy with lactic acidosis and sideroblastic anaemia (MLASA)		
hsa05202	Transcriptional misregulation in cancer - Homo sapiens (human)	Human Diseases; Cancers	861:RUNX1|1436:CSF1R|4353:MPO|1437:CSF2|3562:IL3|862:RUNX1T1|3066:HDAC2|3065:HDAC1|25942:SIN3A|9611:NCOR1|1050:CEBPA|6688:SPI1|929:CD14|3684:ITGAM|2209:FCGR1A|3728:JUP|5371:PML|5914:RARA|1053:CEBPE|597:BCL2A1|7704:ZBTB16|4609:MYC|6929:TCF3|5087:PBX1|51384:WNT16|2120:ETV6|51513:ETV7|1991:ELANE|3002:GZMB|4297:MLL|4299:AFF1|1025:CDK9|905:CCNT2|904:CCNT1|4298:MLLT1|4300:MLLT3|84444:DOT1L|4005:LMO2|5090:PBX3|860:RUNX2|51274:KLF3|4208:MEF2C|221037:JMJD1C|8091:HMGA2|7403:KDM6A|7404:UTY|8464:SUPT3H|8842:PROM1|2322:FLT3|55589:BMP2K|3480:IGF1R|1027:CDKN1B|5218:CDK14|4211:MEIS1|6495:SIX1|51804:SIX4|2138:EYA1|1031:CDKN2C|3248:HPGD|2892:GRIA3|2530:FUT8|30012:TLX3|3195:TLX1|1236:CCR7|8861:LDB1|4066:LYL1|3087:HHEX|171558:PTCRA|5966:REL|7185:TRAF1|598:BCL2L1|942:CD86|958:CD40|604:BCL6|100132941:uncharacterized|100291917:uncharacterized|4094:MAF|894:CCND2|3695:ITGB7|7468:WHSC1|653604:HIST2H3D|8350:HIST1H3A|8352:HIST1H3C|8358:HIST1H3B|8353:HIST1H3E|8356:HIST1H3J|8355:HIST1H3G|8354:HIST1H3I|3021:H3F3B|8357:HIST1H3H|8968:HIST1H3F|8351:HIST1H3D|3020:H3F3A|8290:HIST3H3|126961:HIST2H3C|333932:HIST2H3A|440093:H3F3C|5079:PAX5|7849:PAX8|5468:PPARG|6256:RXRA|6257:RXRB|6258:RXRG|5546:PRCC|7030:TFE3|1026:CDKN1A|7113:TMPRSS2|2078:ERG|5328:PLAU|5327:PLAT|4314:MMP3|4318:MMP9|6692:SPINT1|7850:IL1R2|2115:ETV1|2118:ETV4|2119:ETV5|85414:SLC45A3|2005:ELK4|1655:DDX5|4613:MYCN|4149:MAX|4193:MDM2|5747:PTK2|7157:TP53|648:BMI1|6667:SP1|7709:ZBTB17|4914:NTRK1|4804:NGFR|4221:MEN1|2130:EWSR1|2313:FLI1|3479:IGF1|7048:TGFBR2|3486:IGFBP3|54738:FEV|466:ATF1|9915:ARNT2|472:ATM|64083:GOLPH3|7490:WT1|5154:PDGFA|5155:PDGFB|3560:IL2RB|8938:BAIAP3|7102:TSPAN7|4291:MLF1|8013:NR4A3|8148:TAF15|2521:FUS|1649:DDIT3|1051:CEBPB|3569:IL6|64332:NFKBIZ|4790:NFKB1|5970:RELA|3576:IL8|2308:FOXO1|2321:FLT1|6760:SS18|6756:SSX1|727837:SSX2B|6757:SSX2|26471:NUPR1|79058:ASPSCR1|4233:MET|1668:DEFA3|1848:DUSP6|3205:HOXA9|3206:HOXA10|3207:HOXA11|330:BIRC3|3398:ID2|4086:SMAD1|5077:PAX3|5081:PAX7|6935:ZEB1|8864:PER2|8900:CCNA1	Acute lymphoblastic leukemia (ALL) (precursor B lymphoblastic leukemia)|Acute lymphoblastic leukemia (ALL) (precursor T lymphoblastic leukemia)|Acute myeloid leukemia (AML)|Hairy-cell leukemia|Hodgkin lymphoma|Multiple myeloma|Lymphoplasmacytic lymphoma|Renal cell carcinoma|Prostate cancer|Thyroid cancer|Carcinoid|Ewing's sarcoma|Alveolar rhabdomyosarcoma|Neuroblastoma|Myxoid liposarcoma|Synovial sarcoma|Alveolar soft part sarcoma|Clear cell sarcoma of soft tissue|Extraskeletal myxoid chondrosarcoma|Pituitary adenomas	Lestaurtinib (USAN/INN)	
hsa00120	Primary bile acid biosynthesis - Homo sapiens (human)	Metabolism; Lipid Metabolism	10858:CYP46A1|51302:CYP39A1|80270:HSD3B7|9023:CH25H|9420:CYP7B1|1581:CYP7A1|1593:CYP27A1|1582:CYP8B1|6718:AKR1D1|1109:AKR1C4|10998:SLC27A5|23600:AMACR|8309:ACOX2|3295:HSD17B4|6342:SCP2|10005:ACOT8|570:BAAT	Cerebrotendinous xanthomatosis|Peroxisomal beta-oxidation enzyme deficiency|Familial cholestasis|Congenital bile acid synthesis defect (CBAS)|Leukoencephalopathy with dystonia and motor neuropathy		Bile acids are steroid carboxylic acids derived from cholesterol in vertebrates. The primary bile acids, cholic acid and chenodeoxycholic acid, are synthesized in the liver and conjugated with taurine or glycine before secretion via bile into the intestine. The conversion from cholesterol to cholic and chenodeoxycholic acids involves four steps: 1) the initiation of synthesis by 7alpha-hydroxylation of sterol precursors, 2) further modifications to the ring structures, 3) side-chain oxidation and shortening (cleavage) by three carbons, and 4) conjugation of the bile acid with taurine or glycine.
hsa05164	Influenza A - Homo sapiens (human)	Human Diseases; Infectious Diseases	5646:PRSS3|5645:PRSS2|5644:PRSS1|7113:TMPRSS2|56649:TMPRSS4|4938:OAS1|4940:OAS3|4939:OAS2|6041:RNASEL|3337:DNAJB1|5611:DNAJC3|3306:HSPA2|3310:HSPA6|3304:HSPA1B|3305:HSPA1L|3312:HSPA8|3303:HSPA1A|5610:EIF2AK2|27102:EIF2AK1|440275:EIF2AK4|9451:EIF2AK3|1965:EIF2S1|5606:MAP2K3|5608:MAP2K6|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|6416:MAP2K4|5609:MAP2K7|5602:MAPK10|5601:MAPK9|5599:MAPK8|3725:JUN|1386:ATF2|23586:DDX58|64135:IFIH1|57506:MAVS|79671:NLRX1|3551:IKBKB|4793:NFKBIB|4792:NFKBIA|4790:NFKB1|5970:RELA|7706:TRIM25|7098:TLR3|148022:TICAM1|29110:TBK1|9641:IKBKE|3661:IRF3|1387:CREBBP|2033:EP300|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|207:AKT1|208:AKT2|10000:AKT3|7099:TLR4|51284:TLR7|4615:MYD88|51135:IRAK4|3665:IRF7|3552:IL1A|3553:IL1B|3569:IL6|3592:IL12A|3593:IL12B|7124:TNF|3576:IL8|6347:CCL2|6352:CCL5|3627:CXCL10|3383:ICAM1|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3456:IFNB1|3454:IFNAR1|3455:IFNAR2|3716:JAK1|7297:TYK2|6772:STAT1|6773:STAT2|10379:IRF9|9021:SOCS3|4599:MX1|103:ADAR|5371:PML|3458:IFNG|3459:IFNGR1|3460:IFNGR2|3717:JAK2|4261:CIITA|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|114548:NLRP3|29108:PYCARD|834:CASP1|3606:IL18|90865:IL33|8743:TNFSF10|8793:TNFRSF10D|8794:TNFRSF10C|8795:TNFRSF10B|8797:TNFRSF10A|356:FASLG|355:FAS|7132:TNFRSF1A|7416:VDAC1|54205:CYCS|842:CASP9|2932:GSK3B|3836:KPNA1|3838:KPNA2|7919:DDX39B|7514:XPO1|3267:AGFG1|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|91543:RSAD2|2224:FDPS|60:ACTB|71:ACTG1|10625:IVNS1ABP|10898:CPSF4|390748:PABPN1L|8106:PABPN1|55998:NXF5|56000:NXF3|56001:NXF2|10482:NXF1|728343:NXF2B|55916:NXT2|29107:NXT1|8480:RAE1|11100:HNRNPUL1|4928:NUP98|5045:FURIN|84000:TMPRSS13|5340:PLG|293:SLC25A6|5578:PRKCA|5579:PRKCB	Influenza|Avian influenza		Influenza is a contagious respiratory disease caused by influenza virus infection. Influenza A virus is responsible for both annual seasonal epidemics and periodic worldwide pandemics. Novel strains that cause pandemics arise from avian influenza virus by genetic reassortment among influenza viruses and two surface glycoproteins HA and NA form the basis of serologically distinct virus types. The innate immune system recognizes invaded virus through multiple mechanisms. Viral non-structural NS1 protein is a multifunctional virulence factor that interfere IFN-mediated antiviral response. It inhibits IFN production by blocking activation of transcription factors such as NF-kappa B, IRF3 and AP1. NS1 further inhibits the activation of IFN-induced antiviral genes. PB1-F2 protein is another virulence factor that induce apoptosis of infected cells, which results in life-threatening bronchiolitis.
hsa05150	Staphylococcus aureus infection - Homo sapiens (human)	Human Diseases; Infectious Diseases	2266:FGG|718:C3|629:CFB|1675:CFD|3075:CFH|4153:MBL2|5648:MASP1|10747:MASP2|100132941:uncharacterized|100291917:uncharacterized|712:C1QA|713:C1QB|714:C1QC|715:C1R|716:C1S|717:C2|720:C4A|721:C4B|727:C5|719:C3AR1|728:C5AR1|2209:FCGR1A|9103:FCGR2C|2212:FCGR2A|2213:FCGR2B|2215:FCGR3B|2214:FCGR3A|2204:FCAR|2359:FPR3|2358:FPR2|2357:FPR1|5340:PLG|3426:CFI|6404:SELPLG|6403:SELP|3383:ICAM1|3683:ITGAL|3684:ITGAM|3689:ITGB2|1828:DSG1|3125:HLA-DRB3|3108:HLA-DMA|3111:HLA-DOA|3118:HLA-DQA2|3112:HLA-DOB|3127:HLA-DRB5|3126:HLA-DRB4|3113:HLA-DPA1|3119:HLA-DQB1|3123:HLA-DRB1|3109:HLA-DMB|3117:HLA-DQA1|3115:HLA-DPB1|3122:HLA-DRA|5724:PTAFR|3586:IL10|3858:KRT10	Methicillin-resistant Staphylococcal aureus (MRSA) infection|Vancomycin-resistant Staphylococcal aureus (VRSA) infection		Staphylococcus aureus can cause multiple forms of infections ranging from superficial skin infections to food poisoning and life-threatening infections. The organism has several ways to divert the effectiveness of the immune system: secreting immune modulating proteins that inhibit complement activation and neutrophil chemotaxis or lysis, modulating the sensitivity to cationic antimicrobial peptides (such as defensin) by increasing the positive net charge of its cytoplasmic membrane, and expression of superantigens that prevent development of a normal immune response or cause an emetic response when ingested.
hsa04270	Vascular smooth muscle contraction - Homo sapiens (human)	Organismal Systems; Circulatory System	148:ADRA1A|147:ADRA1B|146:ADRA1D|185:AGTR1|1909:EDNRA|552:AVPR1A|553:AVPR1B|2776:GNAQ|2767:GNA11|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|1579:CYP4A11|284541:CYP4A22|3778:KCNMA1|157855:KCNU1|3779:KCNMB1|10242:KCNMB2|27094:KCNMB3|27345:KCNMB4|775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|4638:MYLK|85366:MYLK2|91807:MYLK3|4637:MYL6|140465:MYL6B|10398:MYL9|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|3708:ITPR1|3709:ITPR2|3710:ITPR3|5579:PRKCB|5578:PRKCA|5582:PRKCG|5588:PRKCQ|5581:PRKCE|5580:PRKCD|5583:PRKCH|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|800:CALD1|59:ACTA2|72:ACTG2|94274:PPP1R14A|5501:PPP1CC|5499:PPP1CA|5500:PPP1CB|4659:PPP1R12A|4660:PPP1R12B|2768:GNA12|10672:GNA13|23365:ARHGEF12|9138:ARHGEF1|9826:ARHGEF11|387:RHOA|6093:ROCK1|9475:ROCK2|135:ADORA2A|136:ADORA2B|5739:PTGIR|10203:CALCRL|10267:RAMP1|10266:RAMP2|10268:RAMP3|2778:GNAS|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|4881:NPR1|4882:NPR2|10335:MRVI1|2982:GUCY1A3|2977:GUCY1A2|2983:GUCY1B3|4629:MYH11|5592:PRKG1	Brugada syndrome (BRS)|Atrial fibrillation|Hypokalemic periodic paralysis (HypoPP)|Familial thoracic aortic aneurysm and dissection (TAAD)	Noradrenaline (JP16)|Adrenaline (JP16)|Vasopressin (JP16/USP)|Epoprostenol (USAN/INN)|Ephedrine (USP)|Carvedilol (JAN/USAN/INN)|Clozapine (JAN/USP/INN)|Desmopressin (INN)|Felodipine (JAN/USP/INN)|Isradipine (USP/INN)|Losartan potassium (JP16/USAN)|Lypressin (USP/INN)|Valsartan (JAN/USAN/INN)|Risperidone (JP16/USAN/INN)|Nifedipine (JP16/USP/INN)|Nimodipine (USAN/INN)|Olanzapine (JAN/USAN/INN)|Quetiapine fumarate (JAN/USAN)|Pseudoephedrine hydrochloride (USP)|Phenoxybenzamine hydrochloride (USP)|Phentolamine mesilate (JAN/INN)|Phenylephrine hydrochloride (JP16/USP)|Candesartan (USAN/INN)|Irbesartan (JAN/USAN/INN)|Anhydrous caffeine (JP16)|Pimozide (JP16/USP/INN)|Sertindole (USAN/INN)|Labetalol hydrochloride (JP16/USP)|Guanadrel sulfate (USP)|Doxazosin mesilate (JP16)|Prazosin hydrochloride (JP16/USP)|Terazosin hydrochloride hydrate (JAN)|Amlodipine besilate (JP16)|Diltiazem hydrochloride (JP16/USP)|Nicardipine hydrochloride (JP16/USAN)|Nisoldipine (JAN/USAN/INN)|Verapamil hydrochloride (JP16/USP)|Candesartan cilexetil (JP16/USAN)|Telmisartan (JAN/USAN/INN)|Nitrendipine (JP16/USAN/INN)|Bepridil hydrochloride hydrate (JAN)|Amiodarone hydrochloride (JP16/USAN)|Ergotamine tartrate (JP16/USP)|Methylergometrine maleate (JP16)|Naphazoline hydrochloride (JP16/USP)|Tetrahydrozoline nitrate (JAN)|Epinephrine hydrochloride (JAN)|Tolazoline hydrochloride (JAN/USP)|Dipivefrin hydrochloride (JAN/USP)|Metaraminol bitartrate (JAN/USP)|Methoxamine hydrochloride (JAN)|Naphazoline nitrate (JP16)|Oxymetazoline hydrochloride (JAN/USP)|Tetrahydrozoline hydrochloride (JAN/USP)|Tamsulosin hydrochloride (JP16/USAN)|Barnidipine hydrochloride (JAN)|Azelnidipine (JAN/INN)|Ergometrine maleate (JP16)|Cilnidipine (JAN/INN)|Pimilprost (JAN/INN)|Olmesartan medoxomil (JAN/USAN)|Bosentan hydrate (JAN)|Conivaptan hydrochloride (JAN/USAN)|Midodrine hydrochloride (JAN/USAN)|Urapidil (JP16/INN)|Epoprostenol sodium (JAN/USAN)|Tramazoline hydrochloride (JAN/USAN)|Mianserin hydrochloride (JAN/USAN)|Bevantolol hydrochloride (JAN/USAN)|Ibudilast (JP16/INN)|Ephedrine hydrochloride (JP16/USP)|Norfenefrine hydrochloride (JAN)|Bunitrolol hydrochloride (JAN)|Ifenprodil tartrate (JP16)|Amosulalol hydrochloride (JP16)|Levomepromazine hydrochloride (JAN/USAN)|Beraprost sodium (JP16/USAN)|Manidipine hydrochloride (JP16)|Aranidipine (JAN/INN)|Moxisylyte hydrochloride (JAN)|Etilefrine hydrochloride (JP16)|Efonidipine hydrochloride ethanolate (JAN)|Naftopidil (JAN/INN)|Alfuzosin hydrochloride (JAN/USAN)|Proxyphylline (JAN/INN)|Arotinolol hydrochloride (JP16)|Bunazosin hydrochloride (JP16)|Nilvadipine (JP16/USAN/INN)|L-Methylephedrine hydrochloride (JAN)|Silodosin (JAN/INN)|Gallopamil hydrochloride (JAN)|Setiptiline maleate (JAN)|Benidipine hydrochloride (JP16)|Clinprost (JAN/INN)|Eprosartan mesylate (USAN)|dl-Methylephedrine hydrochloride (JP16)|Epinephrine bitartrate (JAN/USP)|Dihydroergotamine mesilate (JP16)|Desmopressin acetate hydrate (JAN)|Levomepromazine maleate (JP16/USAN)|Dipivefrin (USAN)|Verapamil (USAN/INN)|Ketanserin (USAN/INN)|Dronedarone (INN)|Beraprost (USAN)|Iloprost (USAN/INN)|Amiodarone (USAN/INN)|Amlodipine maleate (USAN)|Arbutamine hydrochloride (USAN)|Argipressin tannate (USAN)|Asenapine maleate (USAN)|Atrasentan hydrochloride (USAN)|Binodenoson (USAN/INN)|Apadenoson (USAN)|Carvedilol phosphate hydrate (JAN)|Dapiprazole hydrochloride (USAN)|Darodipine (USAN/INN)|Diltiazem malate (USAN)|Dronedarone hydrochloride (USAN)|Edonentan (USAN)|Ephedrine sulfate (USP)|Eprosartan (USAN/INN)|Saralasin acetate (USAN)|Fiduxosin hydrochloride (USAN)|Forasartan (USAN/INN)|Indoramin (USAN/INN)|Indoramin hydrochloride (USAN)|Istradefylline (JAN/USAN/INN)|Lacidipine (USAN/INN)|Medroxalol (USAN/INN)|Medroxalol hydrochloride (USAN)|Nesiritide (USAN/INN)|Nesiritide citrate (USAN)|Norepinephrine bitartrate (USP)|Olmesartan (USAN/INN)|Pelanserin hydrochloride (USAN)|Aminophylline hydrate (JP16)|Pseudoephedrine polistirex (USAN)|Pseudoephedrine sulfate (USP)|Regadenoson (USAN/INN)|Treprostinil (JAN/USAN/INN)|Olanzapine pamoate (USAN)|Terlipressin (USAN/INN)|Ambrisentan (JAN/INN)|Alfuzosin (INN)|Oxedrine (BAN)|Ornipressin (INN)|Amlodipine (INN)|Amosulalol (INN)|Arotinolol (INN)|Barnidipine (INN)|Benidipine (INN)|Bepridil (INN)|Bosentan (INN)|Bunazosin (INN)|Clazosentan sodium (JAN)|Zibotentan (JAN/USAN/INN)|Conivaptan (INN)|Dihydroergotamine (INN)|Dihydroergotamine tartrate|Diltiazem (INN)|Doxazosin (INN)|Efonidipine (INN)|Ergometrine (INN)|Ergotamine (INN)|Etilefrine (INN)|Gallopamil (INN)|Ifenprodil (INN)|Iloprost tromethamine|Azilsartan medoxomil (USAN)|Ketanserin tartrate|Labetalol (INN)|Losartan (INN)|Manidipine (INN)|Metaraminol (INN)|Methylephedrine (BAN)|Methylergometrine (INN)|Mianserin (INN)|Midodrine (INN)|Moxisylyte (INN)|Naphazoline (INN)|Nicardipine (INN)|Norepinephrine hydrochoride|Norfenefrine (INN)|Oxedrine tartrate|Oxedrine hydrochloride|Oxymetazoline (INN)|Phenoxybenzamine (INN)|Phentolamine (INN)|Phenylephrine (INN)|Phenylephrine tartrate|Prazosin (INN)|Pseudoephedrine (INN)|Quetiapine (INN)|Setiptiline (INN)|Tamsulosin (INN)|Terazosin (INN)|Terlipressin acetate (JAN)|Tetryzoline (INN)|Tolazoline (INN)|Tramazoline (INN)|Treprostinil monosodium salt|Urapidil hydrochloride|Azilsartan (JAN/USAN/INN)|Phenylephrine bitartrate (USP)|Norepinephrine hydrochloride (JAN)|Vipadenant (USAN/INN)|Selexipag (JAN/USAN/INN)	The vascular smooth muscle cell (VSMC) is a highly specialized cell whose principal function is contraction. On contraction, VSMCs shorten, thereby decreasing the diameter of a blood vessel to regulate the blood flow and pressure. |The principal mechanisms that regulate the contractile state of VSMCs are changes in cytosolic Ca2+ concentration ([Ca2+]c). In response to vasoconstrictor stimuli, Ca2+ is mobilized from intracellular stores and/or the extracellular space to increase [Ca2+]c in VSMCs. The increase in [Ca2+]c, in turn, activates the Ca2+-CaM-MLCK pathway and stimulates MLC20 phosphorylation, leading to myosin-actin interactions and, hence, the development of contractile force. The sensitivity of contractile myofilaments or MLC20 phosphorylation to Ca2+ can be secondarily modulated by other signaling pathways. During receptor stimulation, the contractile force is greatly enhanced by the inhibition of myosin phosphatase. Rho/Rho kinase, PKC, and arachidonic acid have been proposed to play a pivotal role in this enhancement. |The signaling events that mediate relaxation include the removal of a contractile agonist (passive relaxation) and activation of cyclic nucleotide-dependent signaling pathways in the continued presence of a contractile agonist (active relaxation). Active relaxation occurs through the inhibition of both Ca2+ mobilization and myofilament Ca2+ sensitivity in VSMCs.
hsa04977	Vitamin digestion and absorption - Homo sapiens (human)	Organismal Systems; Digestive System	2346:FOLH1|686:BTD|2694:GIF|8029:CUBN|55788:LMBRD1|25974:MMACHC|4363:ABCC1|6948:TCN2|10560:SLC19A2|80704:SLC19A3|113278:SLC52A3|8884:SLC5A6|6573:SLC19A1|949:SCARB1|5406:PNLIP|151056:PLB1|5948:RBP2|158835:AWAT2|9227:LRAT|337:APOA4|338:APOB|335:APOA1|113235:SLC46A1|9963:SLC23A1	Familial amyloidosis|Hypoalphalipoproteinemia|Biotinidase deficiency|Transcobalamin II deficiency		Vitamins are a diverse and chemically unrelated group of organic substances that share a common feature of being essential for normal health and well-being. They catalyze numerous biochemical reactions. Because humans and other mammals cannot synthesize these compounds (except for some synthesis of niacin), they must obtain them from exogenous sources via intestinal absorption. Vitamins  are classified based on their solubility in water or fat. Most of the water-soluble vitamins are transported across the small intestinal membrane by carrier-mediated mechanisms, but vitamin B12, cobalamin, is transported by a receptor-mediated mechanism. Intestinal absorption of fat-soluble vitamins requires all of the processes needed for fat absorption. After digestion, these vitamins and the products of pancreatic hydrolysis of triglycerides (TG) are emulsified by bile salts to form mixed micelles which are taken up by intestinal enterocytes and incorporated into chylomicrons (CM). CM are then secreted into the lymphatic system, and finally moves into the plasma.
hsa03440	Homologous recombination - Homo sapiens (human)	Genetic Information Processing; Replication and Repair	6742:SSBP1|10111:RAD50|4361:MRE11A|4683:NBN|6117:RPA1|6118:RPA2|6119:RPA3|29935:RPA4|5888:RAD51|5893:RAD52|675:BRCA2|7979:SHFM1|5890:RAD51B|5889:RAD51C|5892:RAD51D|7516:XRCC2|7517:XRCC3|8438:RAD54L|25788:RAD54B|5424:POLD1|5425:POLD2|10714:POLD3|57804:POLD4|641:BLM|7156:TOP3A|8940:TOP3B|80198:MUS81|146956:EME1	DNA repair defects|Defects in RecQ helicases|Ataxia with ocular apraxia (AOA)		Homologous recombination (HR) is essential for the accurate repair of DNA double-strand breaks (DSBs), potentially lethal lesions. HR takes place in the late S-G2 phase of the cell cycle and involves the generation of a single-stranded region of DNA, followed by strand invasion, formation of a Holliday junction, DNA synthesis using the intact strand as a template, branch migration and resolution. It is investigated that RecA/Rad51 family proteins play a central role. The breast cancer susceptibility protein Brca2 and the RecQ helicase BLM (Bloom syndrome mutated) are tumor suppressors that maintain genome integrity, at least in part, through HR.
hsa00780	Biotin metabolism - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	3141:HLCS|686:BTD	Holocarboxylase synthetase deficiency|Brunner syndrome|Biotinidase deficiency		
hsa04320	Dorso-ventral axis formation - Homo sapiens (human)	Organismal Systems; Development	1956:EGFR|2885:GRB2|6654:SOS1|6655:SOS2|3845:KRAS|5604:MAP2K1|5594:MAPK1|5595:MAPK3|2120:ETV6|51513:ETV7|2114:ETS2|2113:ETS1|4854:NOTCH3|4853:NOTCH2|4855:NOTCH4|4851:NOTCH1|64506:CPEB1|55124:PIWIL2|143689:PIWIL4|9271:PIWIL1|440822:PIWIL3|56776:FMN2|56907:SPIRE1|84501:SPIRE2			
hsa04920	Adipocytokine signaling pathway - Homo sapiens (human)	Organismal Systems; Endocrine System	7124:TNF|7132:TNFRSF1A|8717:TRADD|7133:TNFRSF1B|7186:TRAF2|2475:MTOR|5602:MAPK10|5601:MAPK9|5599:MAPK8|1147:CHUK|3551:IKBKB|8517:IKBKG|4792:NFKBIA|4793:NFKBIB|4794:NFKBIE|4790:NFKB1|5970:RELA|9021:SOCS3|8471:IRS4|8660:IRS2|3667:IRS1|207:AKT1|208:AKT2|10000:AKT3|948:CD36|2180:ACSL1|2182:ACSL4|2181:ACSL3|51703:ACSL5|23305:ACSL6|23205:ACSBG1|81616:ACSBG2|3952:LEP|3953:LEPR|3717:JAK2|6774:STAT3|5443:POMC|5562:PRKAA1|5563:PRKAA2|5565:PRKAB2|5564:PRKAB1|5571:PRKAG1|53632:PRKAG3|51422:PRKAG2|181:AGRP|4852:NPY|10891:PPARGC1A|5106:PCK2|5105:PCK1|2538:G6PC|57818:G6PC2|5781:PTPN11|5465:PPARA|6256:RXRA|6257:RXRB|6258:RXRG|9370:ADIPOQ|51094:ADIPOR1|79602:ADIPOR2|6794:STK11|10645:CAMKK2|84254:CAMKK1|1375:CPT1B|1374:CPT1A|126129:CPT1C|6513:SLC2A1|6517:SLC2A4|32:ACACB|5588:PRKCQ	Incontinentia pigmenti|Peutz-Jeghers syndrome|Primary torsion dystonia (PTD)|GLUT1 deficiency syndrome (GLUT1DS)|Cocoon syndrome|Adiponectin deficiency|Metachondromatosis|CD36 deficiency|Wolff-Parkinson-White (WPW) syndrome	Clofibrate (JP16/USP/INN)|Gemfibrozil (JAN/USP/INN)|Fenofibrate (JAN/INN)|Buformin (USAN/INN)|Etanercept (genetical recombination) (JAN)|Metformin hydrochloride (JP16/USP)|Aluminum clofibrate (JAN/INN)|Bezafibrate (JP16/USAN/INN)|Buformin hydrochloride (JP16)|Infliximab (genetical recombination) (JAN)|Bexarotene (USAN/INN)|Certolizumab pegol (genetical recombination) (JAN)|Ciprofibrate (USAN/INN)|Dapiclermin (USAN/INN)|Golimumab (genetical recombination) (JAN)|Metformin (USAN/INN)|Metreleptin (USAN/INN)|Muraglitazar (USAN/INN)|Oxfenicine (USAN/INN)|Theofibrate (USAN)|Etofibrate (INN)|Magnesium clofibrate (INN)|Choline fenofibrate (USAN/INN)	Increased adipocyte volume and number are positively correlated with leptin production, and negatively correlated with production of adiponectin.|Leptin is an important regulator of energy intake and metabolic rate primarily by acting at hypothalamic nuclei. Leptin exerts its anorectic effects by modulating the levels of neuropeptides such as NPY, AGRP, and alpha-MSH. This leptin action is through the JAK kinase, STAT3 phosphorylation, and nuclear transcriptional effect.|Adiponectin lowers plasma glucose and FFAs. These effects are partly accounted for by adiponectin-induced AMPK activation, which in turn stimulates skeletal muscle fatty acid oxidation and glucose uptake. Furthermore, activation of AMPK by adiponectin suppresses endogenous glucose production, concomitantly with inhibition of PEPCK and G6Pase expression.|The proinflammatory cytokine TNFalpha has been implicated as a link between obesity and insulin resistance. TNFalpha interferes with early steps of insulin signaling. Several data have shown that TNFalpha inhibits IRS1 tyrosine phosphorylation by promoting its serine phosphorylation. Among the serine/threonine kinases activated by TNFalpha, JNK, mTOR and IKK have been shown to be involved in this phosphorylation.
hsa00471	D-Glutamine and D-glutamate metabolism - Homo sapiens (human)	Metabolism; Metabolism of Other Amino Acids	2744:GLS|27165:GLS2|2746:GLUD1|2747:GLUD2			
hsa00410	beta-Alanine metabolism - Homo sapiens (human)	Metabolism; Metabolism of Other Amino Acids	2571:GAD1|2572:GAD2|84735:CNDP1|57571:CARNS1|55748:CNDP2|18:ABAT|6723:SRM|6611:SMS|314:AOC2|8639:AOC3|219:ALDH1B1|224:ALDH3A2|217:ALDH2|501:ALDH7A1|223:ALDH9A1|222:ALDH3B2|220:ALDH1A3|221:ALDH3B1|218:ALDH3A1|1806:DPYD|1807:DPYS|51733:UPB1|26275:HIBCH|3030:HADHA|1962:EHHADH|1892:ECHS1|34:ACADM|23417:MLYCD|4329:ALDH6A1	Snyder-Robinson syndrome|Cerebral palsy	Cyanamide (JP16)|Disulfiram (JP16/USP/INN)|Valproic acid (USP)|Vigabatrin (JAN/USAN/INN)|Sodium valproate (JP16)|Gimeracil (JAN/INN)|Calcium valproate	
hsa05212	Pancreatic cancer - Homo sapiens (human)	Human Diseases; Cancers	3845:KRAS|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|9459:ARHGEF6|5879:RAC1|5880:RAC2|5881:RAC3|4790:NFKB1|5970:RELA|207:AKT1|208:AKT2|10000:AKT3|1147:CHUK|3551:IKBKB|8517:IKBKG|572:BAD|598:BCL2L1|842:CASP9|369:ARAF|673:BRAF|5894:RAF1|5604:MAP2K1|5594:MAPK1|5595:MAPK3|5602:MAPK10|5601:MAPK9|5599:MAPK8|5900:RALGDS|5898:RALA|5899:RALB|10928:RALBP1|998:CDC42|7039:TGFA|1950:EGF|1956:EGFR|2064:ERBB2|3716:JAK1|6774:STAT3|6772:STAT1|7423:VEGFB|5228:PGF|7422:VEGFA|7424:VEGFC|2277:FIGF|1029:CDKN2A|1019:CDK4|1021:CDK6|595:CCND1|5925:RB1|1871:E2F3|1869:E2F1|1870:E2F2|7157:TP53|7040:TGFB1|7042:TGFB2|7043:TGFB3|7046:TGFBR1|7048:TGFBR2|4087:SMAD2|4088:SMAD3|4089:SMAD4|675:BRCA2|5888:RAD51|5337:PLD1	Pancreatic cancer	Canertinib dihydrochloride (USAN)|Erlotinib (INN)	Infiltrating ductal adenocarcinoma is the most common malignancy of the pancreas. When most investigators use the term 'pancreatic cancer' they are referring to pancreatic ductal adenocarcinoma (PDA). Normal duct epithelium progresses to infiltrating cancer through a series of histologically defined precursors (PanINs). The overexpression of HER-2/neu and activating point mutations in the K-ras gene occur early, inactivation of the p16 gene at an intermediate stage, and the inactivation of p53, SMAD4, and BRCA2 occur relatively late. Activated K-ras engages multiple effector pathways.  Although EGF receptors are conventionally regarded as upstream activators of RAS proteins, they can also act as RAS signal transducers via RAS-induced autocrine activation of the EGFR family ligands. Moreover, PDA shows extensive genomic instability and aneuploidy. Telomere attrition and mutations in p53 and BRCA2 are likely to contribute to these phenotypes. Inactivation of the SMAD4 tumour suppressor gene leads to loss of the inhibitory influence of the transforming growth factor-beta signalling pathway.
hsa04724	Glutamatergic synapse - Homo sapiens (human)	Organismal Systems; Nervous System	81539:SLC38A1|54407:SLC38A2|2744:GLS|27165:GLS2|57084:SLC17A6|57030:SLC17A7|246213:SLC17A8|2897:GRIK1|2898:GRIK2|2899:GRIK3|2900:GRIK4|2901:GRIK5|2890:GRIA1|2891:GRIA2|2892:GRIA3|2893:GRIA4|2902:GRIN1|2903:GRIN2A|2904:GRIN2B|2905:GRIN2C|2906:GRIN2D|116443:GRIN3A|116444:GRIN3B|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|1742:DLG4|9229:DLGAP1|50944:SHANK1|22941:SHANK2|85358:SHANK3|7220:TRPC1|2911:GRM1|2915:GRM5|9454:HOMER3|9456:HOMER1|9455:HOMER2|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|5579:PRKCB|5578:PRKCA|5582:PRKCG|3708:ITPR1|3709:ITPR2|3710:ITPR3|391013:PLA2G2C|26279:PLA2G2D|30814:PLA2G2E|8399:PLA2G10|5319:PLA2G1B|5322:PLA2G5|50487:PLA2G3|5320:PLA2G2A|123745:PLA2G4E|81579:PLA2G12A|84647:PLA2G12B|64600:PLA2G2F|8681:JMJD7-PLA2G4B|5321:PLA2G4A|8398:PLA2G6|100137049:PLA2G4B|5337:PLD1|5338:PLD2|5594:MAPK1|5595:MAPK3|2778:GNAS|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|2912:GRM2|2913:GRM3|2914:GRM4|2916:GRM6|2918:GRM8|2917:GRM7|2773:GNAI3|2770:GNAI1|2771:GNAI2|2775:GNAO1|2782:GNB1|2783:GNB2|2784:GNB3|59345:GNB4|10681:GNB5|54331:GNG2|2785:GNG3|2786:GNG4|2787:GNG5|2788:GNG7|94235:GNG8|2790:GNG10|2791:GNG11|55970:GNG12|51764:GNG13|2792:GNGT1|2793:GNGT2|156:ADRBK1|157:ADRBK2|3760:KCNJ3|773:CACNA1A|6506:SLC1A2|6512:SLC1A7|6505:SLC1A1|6511:SLC1A6|775:CACNA1C|776:CACNA1D|6507:SLC1A3|2752:GLUL|10991:SLC38A3	Syndromic X-linked mental retardation with epilepsy or seizures|Episodic ataxias|Nonsyndromic autosomal recessive mental retardation (NS-ARMR)|Familial or sporadic hemiplegic migraine|Congenital stationary night blindness (CSNB)|Dicarboxylic aminoaciduria|Congenital systemic glutamine deficiency (CSGD)	Topiramate (JAN/USAN/INN)|Ketamine hydrochloride (JP16/USP)|Amantadine hydrochloride (JP16/USP)|Dextromethorphan hydrobromide hydrate (JP16)|Selfotel (USAN/INN)|Kainic acid hydrate (JP16)|Talampanel (INN)|Aptiganel hydrochloride (USAN)|Besonprodil (USAN)|Delucemine hydrochloride (USAN)|Dextromethorphan (USP)|Dextromethorphan polistirex (USAN)|Dextrorphan hydrochloride (USAN)|Dizocilpine maleate (USAN)|Eglumetad (USAN)|Fenobam (USAN)|Gavestinel (USAN/INN)|Licostinel (USAN/INN)|Memantine hydrochloride (JAN/USAN)|Neramexane mesylate (USAN)|Perzinfotel (USAN/INN)|Phencyclidine hydrochloride (USAN)|Remacemide hydrochloride (USAN)|Traxoprodil mesylate (USAN)|Esketamine (INN)|Amantadine (INN)|Ifenprodil (INN)|Ketamine (INN)|Levomethadone (INN)|Levomethadone hydrochloride|Memantine (INN)|Methadone (BAN)|Eglumegad (INN)|Pomaglumetad methionil (USAN/INN)	Glutamate is the major excitatory neurotransmitter in the mammalian central nervous system(CNS). Glutamate is packaged into synaptic vesicles in the presynaptic terminal. Once released into the synaptic cleft,  glutamate acts on postsynaptic ionotropic glutamate receptors (iGluRs) to mediate fast excitatory synaptic transmission. Glutamate can also act on metabotropic glutamate receptors (mGluRs) and exert a variety of modulatory effects through their coupling to G proteins and the subsequent recruitment of second messenger systems. Presynaptically localized Group II and Group III mGluRs are thought to represent the classical inhibitory autoreceptor mechanism that suppresses excess glutamate release. After its action on these receptors, glutamate can be removed from the synaptic cleft by EAATs located either on the presynaptic terminal, neighboring glial cells, or the postsynaptic neuron. In glia, glutamate is converted to glutamine, which is then transported back to the presynaptic terminal and converted back to glutamate.
hsa05169	Epstein-Barr virus infection - Homo sapiens (human)	Human Diseases; Infectious Diseases	10000:AKT3|100132941:uncharacterized|10014:HDAC5|100291917:uncharacterized|1017:CDK2|10213:PSMD14|1026:CDKN1A|1027:CDKN1B|10454:TAB1|10621:POLR3F|10622:POLR3G|10623:POLR3C|10971:YWHAQ|11128:POLR3A|11317:RBPJL|1147:CHUK|1380:CR2|1386:ATF2|1387:CREBBP|1432:MAPK14|1457:CSNK2A1|1459:CSNK2A2|1460:CSNK2B|171568:POLR3H|2033:EP300|207:AKT1|208:AKT2|2208:FCER2|2268:FGR|22938:SNW1|23118:TAB2|23533:PIK3R5|23586:DDX58|246721:POLR2J2|26993:AKAP8L|27044:SND1|27102:EIF2AK1|29110:TBK1|2932:GSK3B|2959:GTF2B|2960:GTF2E1|2961:GTF2E2|3065:HDAC1|3066:HDAC2|3105:HLA-A|3106:HLA-B|3107:HLA-C|3113:HLA-DPA1|3115:HLA-DPB1|3117:HLA-DQA1|3118:HLA-DQA2|3119:HLA-DQB1|3122:HLA-DRA|3123:HLA-DRB1|3125:HLA-DRB3|3126:HLA-DRB4|3127:HLA-DRB5|3133:HLA-E|3134:HLA-F|3135:HLA-G|3303:HSPA1A|3304:HSPA1B|3305:HSPA1L|3306:HSPA2|3310:HSPA6|3312:HSPA8|3315:HSPB1|3316:HSPB2|3383:ICAM1|3458:IFNG|3516:RBPJ|3551:IKBKB|3586:IL10|3587:IL10RA|3588:IL10RB|3654:IRAK1|3661:IRF3|3683:ITGAL|3716:JAK1|3718:JAK3|3725:JUN|377841:ENTPD8|387332:TBPL2|4067:LYN|4193:MDM2|440275:EIF2AK4|4609:MYC|4734:NEDD4|4790:NFKB1|4791:NFKB2|4792:NFKBIA|4793:NFKBIB|4794:NFKBIE|51082:POLR1D|51728:POLR3K|5290:PIK3CA|5291:PIK3CB|5293:PIK3CD|5294:PIK3CG|5295:PIK3R1|5296:PIK3R2|5335:PLCG1|5336:PLCG2|5430:POLR2A|5431:POLR2B|5432:POLR2C|5433:POLR2D|5434:POLR2E|5435:POLR2F|5436:POLR2G|5437:POLR2H|5438:POLR2I|5439:POLR2J|5440:POLR2K|5441:POLR2L|548644:POLR2J3|5566:PRKACA|5567:PRKACB|5568:PRKACG|55703:POLR3B|55718:POLR3E|5599:MAPK8|5600:MAPK11|5601:MAPK9|5602:MAPK10|5603:MAPK13|5606:MAP2K3|5608:MAP2K6|5609:MAP2K7|5610:EIF2AK2|5613:PRKX|5700:PSMC1|5701:PSMC2|5702:PSMC3|5704:PSMC4|5705:PSMC5|5706:PSMC6|5707:PSMD1|5708:PSMD2|5709:PSMD3|5710:PSMD4|5713:PSMD7|5714:PSMD8|5717:PSMD11|5718:PSMD12|5719:PSMD13|5757:PTMA|5901:RAN|5925:RB1|596:BCL2|5970:RELA|5971:RELB|6300:MAPK12|6416:MAP2K4|6502:SKP2|661:POLR3D|6688:SPI1|6693:SPN|6774:STAT3|683:BST1|6850:SYK|6885:MAP3K7|6908:TBP|7128:TNFAIP3|7157:TP53|7185:TRAF1|7186:TRAF2|7187:TRAF3|7188:TRAF5|7189:TRAF6|7297:TYK2|7431:VIM|7514:XPO1|7529:YWHAB|7531:YWHAE|7532:YWHAG|7533:YWHAH|7534:YWHAZ|7874:USP7|7979:SHFM1|8021:NUP214|84265:POLR3GL|8503:PIK3R3|8517:IKBKG|8717:TRADD|8737:RIPK1|890:CCNA2|8900:CCNA1|9020:MAP3K14|930:CD19|9451:EIF2AK3|9519:TBPL1|952:CD38|953:ENTPD1|9533:POLR1C|956:ENTPD3|958:CD40|960:CD44|9612:NCOR2|965:CD58|9759:HDAC4|983:CDK1|9861:PSMD6	Infectious mononucleosis		Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus that is associated with oncogenesis. EBV infection to primary human B lymphocytes leads to induction of EBV-specific HLA-restricted cytotoxic T cells, causing infectious mononucleosis during adolescence. Primary infection with EBV is followed by latent infection in which the reservoir B cells are immortalized. EBV tumorigenic potential in Burkitt lymphoma, nasopharyngeal carcinoma, Hodgkin lymphoma, and post-transplant B cell lymphomas has been well-documented. Distinct forms of EBV latency and patterns of latent gene expression can contribute to the different tumours.
hsa05146	Amoebiasis - Homo sapiens (human)	Human Diseases; Infectious Diseases	3553:IL1B|3554:IL1R1|7850:IL1R2|4790:NFKB1|5970:RELA|3315:HSPB1|4583:MUC2|1280:COL2A1|1302:COL11A2|1301:COL11A1|1277:COL1A1|1289:COL5A1|50509:COL5A3|1281:COL3A1|1290:COL5A2|1278:COL1A2|1284:COL4A2|1286:COL4A4|1288:COL4A6|1287:COL4A5|1282:COL4A1|2335:FN1|284217:LAMA1|3908:LAMA2|3911:LAMA5|3909:LAMA3|3910:LAMA4|3912:LAMB1|3913:LAMB2|3914:LAMB3|22798:LAMB4|3915:LAMC1|3918:LAMC2|10319:LAMC3|836:CASP3|100132941:uncharacterized|100291917:uncharacterized|2776:GNAQ|2767:GNA11|9630:GNA14|2769:GNA15|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|5579:PRKCB|5578:PRKCA|5582:PRKCG|2778:GNAS|2774:GNAL|107:ADCY1|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|5868:RAB5A|5869:RAB5B|5878:RAB5C|7879:RAB7A|338382:RAB7B|7097:TLR2|7099:TLR4|929:CD14|3569:IL6|1437:CSF2|3576:IL8|7124:TNF|3592:IL12A|3593:IL12B|3458:IFNG|5747:PTK2|7414:VCL|81:ACTN4|88:ACTN2|87:ACTN1|89:ACTN3|383:ARG1|384:ARG2|4843:NOS2|3689:ITGB2|3684:ITGAM|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|6318:SERPINB4|5272:SERPINB9|5273:SERPINB10|5275:SERPINB13|5269:SERPINB6|1992:SERPINB1|5055:SERPINB2|6317:SERPINB3|1511:CTSG|3586:IL10|7040:TGFB1|7042:TGFB2|7043:TGFB3|731:C8A|732:C8B|733:C8G|735:C9|2919:CXCL1|912:CD1D	Amoebiasis		Entamoeba histolytica, an extracellular protozoan parasite is a human pathogen that invades the intestinal epithelium. Infection occurs on ingestion of contaminated water and food. The pathogenesis of amoebiasis begins with parasite attachment and disruption of the intestinal mucus layer, followed by apoptosis of host epithelial cells. Intestinal tissue destruction causes severe dysentery and ulcerations in amoebic colitis. Several amoebic proteins such as lectins, cysteine proteineases, and amoebapores are associated with the invasion process. The parasite can cause extraintestinal infection like amoebic liver abscess by evading immune response.
hsa04020	Calcium signaling pathway - Homo sapiens (human)	Environmental Information Processing; Signal Transduction	6547:SLC8A3|6546:SLC8A1|6543:SLC8A2|491:ATP2B2|490:ATP2B1|493:ATP2B4|492:ATP2B3|1128:CHRM1|1131:CHRM3|1133:CHRM5|135:ADORA2A|136:ADORA2B|153:ADRB1|154:ADRB2|155:ADRB3|1812:DRD1|1816:DRD5|3274:HRH2|3360:HTR4|3361:HTR5A|3362:HTR6|3363:HTR7|2778:GNAS|2774:GNAL|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|5350:PLN|488:ATP2A2|489:ATP2A3|487:ATP2A1|7220:TRPC1|775:CACNA1C|776:CACNA1D|778:CACNA1F|779:CACNA1S|773:CACNA1A|774:CACNA1B|777:CACNA1E|8913:CACNA1G|8912:CACNA1H|8911:CACNA1I|1139:CHRNA7|5023:P2RX1|22953:P2RX2|5024:P2RX3|5025:P2RX4|5026:P2RX5|5027:P2RX7|9127:P2RX6|2902:GRIN1|2903:GRIN2A|2905:GRIN2C|2906:GRIN2D|6261:RYR1|6262:RYR2|6263:RYR3|10800:CYSLTR1|57105:CYSLTR2|1129:CHRM2|148:ADRA1A|147:ADRA1B|146:ADRA1D|185:AGTR1|1909:EDNRA|1910:EDNRB|2149:F2R|2911:GRM1|2915:GRM5|2925:GRPR|3269:HRH1|3358:HTR2C|3357:HTR2B|3356:HTR2A|3973:LHCGR|4923:NTSR1|5021:OXTR|552:AVPR1A|553:AVPR1B|56413:LTB4R2|5724:PTAFR|5731:PTGER1|5733:PTGER3|5737:PTGFR|623:BDKRB1|624:BDKRB2|6869:TACR1|6865:TACR2|6870:TACR3|6915:TBXA2R|7201:TRHR|886:CCKAR|887:CCKBR|1956:EGFR|2064:ERBB2|2065:ERBB3|2066:ERBB4|5156:PDGFRA|5159:PDGFRB|2776:GNAQ|2767:GNA11|9630:GNA14|2769:GNA15|100132941:uncharacterized|100291917:uncharacterized|84812:PLCD4|113026:PLCD3|5333:PLCD1|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|5335:PLCG1|5336:PLCG2|51196:PLCE1|89869:PLCZ1|3708:ITPR1|3709:ITPR2|3710:ITPR3|683:BST1|952:CD38|8877:SPHK1|56848:SPHK2|7416:VDAC1|7417:VDAC2|7419:VDAC3|292:SLC25A5|293:SLC25A6|291:SLC25A4|83447:SLC25A31|7134:TNNC1|7125:TNNC2|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|5261:PHKG2|5260:PHKG1|5256:PHKA2|5257:PHKB|5255:PHKA1|4638:MYLK|85366:MYLK2|91807:MYLK3|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|814:CAMK4|5530:PPP3CA|5532:PPP3CB|5533:PPP3CC|5534:PPP3R1|63928:CHP2|5535:PPP3R2|11261:CHP|4842:NOS1|4843:NOS2|4846:NOS3|5136:PDE1A|5137:PDE1C|5153:PDE1B|2185:PTK2B|3706:ITPKA|3707:ITPKB|5579:PRKCB|5578:PRKCA|5582:PRKCG|10105:PPIF	46,XY disorders of sex development (Disorders in androgen synthesis or action)|Premature ovarian failure|Central core disease|Darier disease|Brugada syndrome (BRS)|Hypokalemic periodic paralysis (HypoPP)|Episodic ataxias|Acrokeratosis verruciformis|Waardenburg syndrome (WS)|Familial or sporadic hemiplegic migraine|Congenital stationary night blindness (CSNB)|Familial thoracic aortic aneurysm and dissection (TAAD)|ABCD syndrome|Lethal congenital contractural syndrome (LCCS)|Hirschsprung disease (HD)|Precocious puberty|Catecholaminergic polymorphic ventricular tachycardia|Progressive external ophthalmoplegia (PEO)|Brody myopathy	Levodopa (JP16/USP/INN)|Noradrenaline (JP16)|Dinoprost (JP16/USAN/INN)|Oxytocin (JP16/USP/INN)|Adrenaline (JP16)|Vasopressin (JP16/USP)|Atropine (USP)|Ephedrine (USP)|Scopolamine (INN)|Hyoscyamine (USP)|Protirelin (JP16/USAN/INN)|Alprostadil (JP16/USP/INN)|Methyloctatropine bromide (JAN)|Astemizole (JAN/USP/INN)|Atenolol (JP16/USP/INN)|Carvedilol (JAN/USAN/INN)|Chlorpromazine (USP/INN)|Cisapride (USAN/INN)|Clozapine (JAN/USP/INN)|Desmopressin (INN)|Cimetidine (JP16/USP/INN)|Diphenhydramine (JP16/INN)|Divalproex sodium (USP)|Famotidine (JP16/USP/INN)|Felodipine (JAN/USP/INN)|Isradipine (USP/INN)|Latanoprost (JAN/USAN/INN)|Losartan potassium (JP16/USAN)|Loratadine (JAN/USAN/INN)|Lypressin (USP/INN)|Tiotixene (JAN)|Timolol (USAN)|Tropicamide (JP16/USP/INN)|Valproic acid (USP)|Valsartan (JAN/USAN/INN)|Levomepromazine (USAN/INN)|Zafirlukast (JAN/USAN/INN)|Ranitidine (USAN/INN)|Risperidone (JP16/USAN/INN)|Nadolol (JP16/USP/INN)|Nifedipine (JP16/USP/INN)|Nimodipine (USAN/INN)|Nizatidine (JP16/USP/INN)|Olanzapine (JAN/USAN/INN)|Quetiapine fumarate (JAN/USAN)|Oxybutynin (USAN/INN)|Promethazine hydrochloride (JP16/USP)|Propantheline bromide (JP16/USP/INN)|Propranolol hydrochloride (JP16/USP)|Pseudoephedrine hydrochloride (USP)|Promethazine (JAN/INN)|Pergolide mesilate (JAN)|Phenoxybenzamine hydrochloride (USP)|Phentolamine mesilate (JAN/INN)|Phenylephrine hydrochloride (JP16/USP)|Pindolol (JP16/USP/INN)|Dimenhydrinate (JP16/USP/INN)|Terfenadine (JAN/USAN/INN)|Candesartan (USAN/INN)|Irbesartan (JAN/USAN/INN)|Carbachol (JAN/USP/INN)|Pilocarpine (JAN/USP)|Anhydrous caffeine (JP16)|Montelukast sodium (JAN/USAN)|Topiramate (JAN/USAN/INN)|Zonisamide (JAN/USAN/INN)|Ethosuximide (JP16/USP/INN)|Glycopyrronium bromide (JAN/INN)|Pimozide (JP16/USP/INN)|Sertindole (USAN/INN)|Mirtazapine (JAN/USAN/INN)|Acebutolol hydrochloride (JP16/USP)|Betaxolol hydrochloride (JP16/USP)|Carteolol hydrochloride (JP16/USP)|Labetalol hydrochloride (JP16/USP)|Metoprolol tartrate (JP16/USP)|Penbutolol sulfate (JP16/USP)|Timolol maleate (JP16/USP)|Guanadrel sulfate (USP)|Doxazosin mesilate (JP16)|Prazosin hydrochloride (JP16/USP)|Terazosin hydrochloride hydrate (JAN)|Mecamylamine hydrochloride (USP)|Fenoldopam mesylate (USP)|Amlodipine besilate (JP16)|Diltiazem hydrochloride (JP16/USP)|Nicardipine hydrochloride (JP16/USAN)|Nisoldipine (JAN/USAN/INN)|Verapamil hydrochloride (JP16/USP)|Candesartan cilexetil (JP16/USAN)|Telmisartan (JAN/USAN/INN)|Nitrendipine (JP16/USAN/INN)|Bepridil hydrochloride hydrate (JAN)|Dobutamine hydrochloride (JP16/USP)|Dopamine hydrochloride (JP16/USP)|Bisoprolol fumarate (JP16/USP)|Metoprolol succinate (USP)|Amiodarone hydrochloride (JP16/USAN)|Esmolol hydrochloride (JAN/USAN)|Tolterodine (USAN/INN)|Azelastine hydrochloride (JP16/USAN)|Cevimeline hydrochloride hydrate (JAN)|Azatadine maleate (USP)|Brompheniramine maleate (USAN)|Cetirizine hydrochloride (JP16/USAN)|Chlorpheniramine maleate (JP16/USP)|Clemastine fumarate (JP16/USP)|d-Chlorpheniramine maleate (JP16)|Diphenhydramine hydrochloride (JP16/USP)|Fexofenadine hydrochloride (JP16/USAN)|Hydroxyzine hydrochloride (JP16/USP)|Ranitidine hydrochloride (JP16/USP)|Ergotamine tartrate (JP16/USP)|Methylergometrine maleate (JP16)|Carboprost tromethamine (USP)|Salbutamol sulfate (JP16)|Bitolterol mesilate (JAN)|Orciprenaline sulfate (JP16)|Pirbuterol acetate (USAN)|Salmeterol xinafoate (JAN/USAN)|Terbutaline sulfate (JP16/USP)|Sodium valproate (JP16)|Ketamine hydrochloride (JP16/USP)|Hyoscine methobromide (INN)|Dicyclomine hydrochloride (JAN/USP)|Hyoscyamine sulfate (USP)|Mepenzolate bromide (JP16/INN)|Methanthelinium bromide (INN)|Oxybutynin hydrochloride (JAN)|Tridihexethyl chloride (BAN)|Metoclopramide (JP16/INN)|Procaine hydrochloride (JP16/USP)|Naphazoline hydrochloride (JP16/USP)|Tetrahydrozoline nitrate (JAN)|Orphenadrine citrate (USP)|Amantadine hydrochloride (JP16/USP)|Benztropine mesilate (JAN)|Biperiden (JAN/USP/INN)|Procyclidine hydrochloride (USP)|Trihexyphenidyl hydrochloride (JP16/USP)|Chlorpromazine hydrochloride (JP16/USP)|Nefazodone hydrochloride (USAN)|Trazodone hydrochloride (JAN/USP)|Dextromethorphan hydrobromide hydrate (JP16)|Epinephrine hydrochloride (JAN)|Tolazoline hydrochloride (JAN/USP)|Acetylcholine chloride (JP16/USP/INN)|Bethanechol chloride (JP16/USP)|Cyclopentolate hydrochloride (JP16/USP)|Hexocyclium metilsulfate (INN)|Homatropine hydrobromide (JP16/USP)|Isopropamide iodide (JAN/USP/INN)|Oxyphencyclimine hydrochloride (JAN)|Propiverine hydrochloride (JP16)|Dipivefrin hydrochloride (JAN/USP)|Metaraminol bitartrate (JAN/USP)|Methoxamine hydrochloride (JAN)|Naphazoline nitrate (JP16)|Oxymetazoline hydrochloride (JAN/USP)|Tetrahydrozoline hydrochloride (JAN/USP)|Tamsulosin hydrochloride (JP16/USAN)|Levobunolol hydrochloride (JAN/USP)|Sotalol hydrochloride (JAN/USP)|Flupentixol (INN)|Spiperone (JAN/USAN)|Atropine methonitrate (JAN/INN)|Hydroxyzine pamoate (JP16/USP)|Trospium chloride (JAN/USAN/INN)|Barnidipine hydrochloride (JAN)|Profenamine hydrochloride (JAN)|Seratrodast (JAN/USAN/INN)|Ramatroban (JAN/INN)|Lafutidine (JAN/INN)|Isothipendyl hydrochloride (JAN)|Azelnidipine (JAN/INN)|Tolterodine tartrate (JAN/USAN)|Ergometrine maleate (JP16)|Aripiprazole (JAN/USAN/INN)|Piperidolate hydrochloride (JAN)|Diphenylpyraline hydrochloride (JAN)|Cilnidipine (JAN/INN)|Pheniramine maleate (JAN/USP)|Carpronium chloride (JAN/INN)|Blonanserin (JAN/INN)|Alprenolol hydrochloride (JP16/USAN)|Olopatadine hydrochloride (JAN/USAN)|Osutidine (JAN/INN)|Tiemonium iodide (JAN/INN)|Olmesartan medoxomil (JAN/USAN)|Bosentan hydrate (JAN)|Piroheptine hydrochloride (JAN)|Conivaptan hydrochloride (JAN/USAN)|Promethazine teoclate (JAN/INN)|Ritodrine hydrochloride (JP16/USP)|Solifenacin succinate (JAN/USAN/INN)|Cinnarizine (JAN/USAN/INN)|Pirenzepine hydrochloride (USAN)|Flunarizine hydrochloride (JAN/USAN)|Midodrine hydrochloride (JAN/USAN)|Methylbenactyzium bromide (JP16/INN)|Meclizine hydrochloride (JAN/USP)|Zotepine (JAN/INN)|Mequitazine (JP16/INN)|Ketotifen fumarate (JP16/USAN)|Urapidil (JP16/INN)|Carbinoxamine maleate (JAN/USP)|Dimetindene maleate (JAN)|Tramazoline hydrochloride (JAN/USAN)|Pirbuterol hydrochloride (JAN/USAN)|Dinoprost tromethamine (JAN/USP)|Mianserin hydrochloride (JAN/USAN)|Etomidoline (JAN/INN)|Clenbuterol hydrochloride (JAN/USP)|Tulobuterol hydrochloride (JP16)|Bevantolol hydrochloride (JAN/USAN)|Formoterol fumarate (USAN)|Prifinium bromide (JAN/INN)|Ephedrine hydrochloride (JP16/USP)|dl-Isoprenaline hydrochloride (JAN)|Norfenefrine hydrochloride (JAN)|Fenoterol hydrobromide (JAN)|Imatinib mesilate (JAN)|Bunitrolol hydrochloride (JAN)|Ifenprodil tartrate (JP16)|Scopolamine butylbromide (JP16)|Isopropyl unoprostone (JAN)|Bupranolol hydrochloride (JP16)|Homochlorcyclizine hydrochloride (JP16)|Diponium bromide (JAN/INN)|Roxatidine acetate hydrochloride (JP16/USAN)|Amosulalol hydrochloride (JP16)|Esatenolol (JAN/INN)|Ebastine (JP16/USAN/INN)|Pipamperone hydrochloride (JAN)|Butropium bromide (JP16/INN)|Trimebutine maleate (JP16)|Bufetolol hydrochloride (JP16)|Befunolol hydrochloride (JAN)|Levomepromazine hydrochloride (JAN/USAN)|Pipethanate hydrochloride (JAN)|Valethamate bromide (JAN)|Nylidrin hydrochloride (JAN)|Mosapramine hydrochloride (JAN)|Manidipine hydrochloride (JP16)|Aranidipine (JAN/INN)|Moxisylyte hydrochloride (JAN)|Etilefrine hydrochloride (JP16)|Mabuterol hydrochloride (JAN)|Diphenylpiperidinomethyldioxolan iodide (JAN)|Efonidipine hydrochloride ethanolate (JAN)|Sarpogrelate hydrochloride (JP16)|Diphenylpyraline teoclate (JAN)|Methoxyphenamine hydrochloride (JAN)|Hyoscyamine methylbromide (JAN)|Bepotastine besilate (JAN)|Naftopidil (JAN/INN)|Nipradilol (JAN/INN)|Alfuzosin hydrochloride (JAN/USAN)|Dalcotidine (JAN/INN)|Darifenacin hydrobromide (JAN/USAN)|Epinastine hydrochloride (JAN)|Levocabastine hydrochloride (JAN/USAN)|Celiprolol hydrochloride (JAN/USAN)|Clebopride malate (JP16)|Isoxsuprine hydrochloride (JP16/USP)|Proxyphylline (JAN/INN)|Oxatomide (JAN/USAN/INN)|Triprolidine hydrochloride hydrate (JAN)|Bopindolol malonate (JAN)|Oxprenolol hydrochloride (JP16/USP)|Oxapium iodide (JP16/INN)|Proglumide (JP16/USAN/INN)|Arotinolol hydrochloride (JP16)|Landiolol hydrochloride (JAN)|Panazepide (JAN)|Pibutidine hydrochloride (JAN)|Ornoprostil (JAN/INN)|Metixene hydrochloride (JAN)|Tiquizium bromide (JAN/INN)|Bunazosin hydrochloride (JP16)|Dimetotiazine mesilate (JAN)|Nilvadipine (JP16/USAN/INN)|Taltirelin hydrate (JAN)|Tiotropium bromide hydrate (JAN)|Ziprasidone hydrochloride hydrate (JAN)|Oxitropium bromide (JAN/INN)|L-Methylephedrine hydrochloride (JAN)|Aclatonium napadisilate (JAN)|Travoprost (JAN/USAN/INN)|Silodosin (JAN/INN)|Gallopamil hydrochloride (JAN)|N-Methylscopolamine methylsulfate (JAN)|Gefitinib (JAN/USAN/INN)|Trimetoquinol hydrochloride|Pipethanate ethobromide (JAN)|Mosapride citrate hydrate (JP16)|Apomorphine hydrochloride hydrate (JAN)|Protirelin tartrate hydrate (JP16)|Setiptiline maleate (JAN)|Benidipine hydrochloride (JP16)|Isoprenaline sulfate (JAN)|Atropine sulfate (JP16/USP)|Homatropine methylbromide (USP)|Scopolamine hydrobromide hydrate (JP16)|Gemeprost (JAN/USAN/INN)|Metipranolol hydrochloride|Eprosartan mesylate (USAN)|Cyclizine lactate (BAN)|Tripelennamine hydrochloride (USP)|Cisapride (JAN)|Isoetharine hydrochloride (USP)|Ziprasidone mesylate (USAN)|Methadone hydrochloride (USP)|dl-Methylephedrine hydrochloride (JP16)|Albuterol (USP)|Phenindamine tartrate (USAN)|Epinephrine bitartrate (JAN/USP)|l-Isoprenaline hydrochloride (JP16)|Tulobuterol (JAN/INN)|Pilocarpine hydrochloride (JP16/USP)|Hexamethonium bromide (JAN/INN)|Dihydroergotamine mesilate (JP16)|Ipratropium bromide hydrate (JP16)|Metoclopramide hydrochloride (JAN)|Cyproheptadine hydrochloride (JP16/USP)|Desmopressin acetate hydrate (JAN)|Flupentixol dihydrochloride (JAN)|Alimemazine tartrate (JP16)|Biperiden hydrochloride (JP16/USP)|Biperiden lactate (JAN/USP)|Levomepromazine maleate (JP16/USAN)|Emedastine difumarate (JAN/USP)|Levalbuterol hydrochloride (USAN)|Doxylamine succinate (USP)|Acebutolol (USAN/INN)|Bisoprolol (JAN/USAN/INN)|Carboprost (USAN/INN)|Dipivefrin (USAN)|Verapamil (USAN/INN)|Metoprolol (USAN/INN)|Ritodrine (USAN/INN)|Ketanserin (USAN/INN)|Perospirone hydrochloride hydrate (JAN)|Metipranolol (USAN/INN)|Verlukast (USAN/INN)|Primidolol (USAN/INN)|Hexoprenaline sulfate (USAN)|Procaterol hydrochloride (USAN)|Selfotel (USAN/INN)|Flutropium bromide (JAN)|Diphenhydramine salicylate (JAN)|Timepidium bromide hydrate (JP16)|Dronedarone (INN)|Flibanserin (USAN/INN)|Agomelatine (INN)|Montirelin (INN)|Orphenadrine hydrochloride|Thiothixene hydrochloride (USP)|Clopenthixol (USAN)|Denopamine (JAN/INN)|Pipamperone (USAN/INN)|Penfluridol (USAN/INN)|Butaclamol hydrochloride (USAN)|Iloperidone (USAN/INN)|Oxiperomide (USAN/INN)|Human menopausal gonadotrophin (JP16)|Devazepide (USAN/INN)|Talibegron hydrochloride (USAN)|Alprostadil alfadex (JP16)|Tarazepide (INN)|Rosaprostol (INN)|Limaprost (INN)|Tegaserod maleate (USAN)|Pranlukast hydrate (JAN)|Ablukast (USAN/INN)|Ablukast sodium (USAN)|Aceclidine (USAN/INN)|Acrivastine (USAN/INN)|Adatanserin hydrochloride (USAN)|Adrogolide hydrochloride (USAN)|Alprenoxime hydrochloride (USAN)|Altanserin tartrate (USAN)|Cinalukast (USAN/INN)|Pobilukast edamine (USAN)|Ritolukast (USAN/INN)|Tomelukast (USAN/INN)|Limaprost alfadex (JP16)|Alvameline maleate (USAN)|Amesergide (USAN/INN)|Amiodarone (USAN/INN)|Amlodipine maleate (USAN)|Antazoline phosphate (USP)|Aprepitant (JAN/USAN/INN)|Aptiganel hydrochloride (USAN)|Arbutamine hydrochloride (USAN)|Arformoterol tartrate (USAN)|Argipressin tannate (USAN)|Asenapine maleate (USAN)|Atosiban (USAN/INN)|Atrasentan hydrochloride (USAN)|Atropine oxide hydrochloride (USAN)|Becaplermin (USAN/INN)|Benzetimide hydrochloride (USAN)|Besonprodil (USAN)|Binodenoson (USAN/INN)|Bucindolol hydrochloride (USAN)|Bunolol hydrochloride (USAN)|Butopamine (USAN/INN)|Butoxamine hydrochloride (USAN)|Apadenoson (USAN)|Axitinib (JAN/USAN)|Befetupitant (USAN/INN)|Mazaticol hydrochloride hydrate (JAN)|Chlorpromazine hibenzate (JAN)|Profenamine hibenzate (JAN)|Diphenhydramine tannate (JP16)|Promethazine methylenedisalicylate (JAN)|Canertinib dihydrochloride (USAN)|Diphenhydramine laurylsulfate (JAN)|Carboprost methyl (USAN)|Carbuterol hydrochloride (USAN)|Carvedilol phosphate hydrate (JAN)|Cetamolol hydrochloride (USAN)|Cetuximab (genetical recombination) (JAN)|Chlorpheniramine polistirex (USAN)|Choriogonadotropin alfa (USAN/INN)|Cicloprolol hydrochloride (USAN)|Ciladopa hydrochloride (USAN)|Cimaterol (USAN/INN)|Cimetidine hydrochloride (USP)|Cinanserin hydrochloride (USAN)|Clebopride (USAN)|Clemastine (USAN)|Zuclopenthixol (INN)|Colterol mesylate (USAN)|Cyclizine (INN)|Cyclizine hydrochloride (USP)|Daltroban (USAN/INN)|Dapiprazole hydrochloride (USAN)|Darifenacin (USAN/INN)|Darodipine (USAN/INN)|Dasatinib (INN)|Deltibant (USAN/INN)|Delucemine hydrochloride (USAN)|Desloratadine (USAN/INN)|Dexbrompheniramine maleate (USAN)|Dexetimide (USAN/INN)|Dexfenfluramine hydrochloride (USAN)|Dexpropranolol hydrochloride (USAN)|Dextromethorphan (USP)|Dextromethorphan polistirex (USAN)|Dextrorphan hydrochloride (USAN)|Diacetolol hydrochloride (USAN)|Atropine methylbromide (JAN)|Diltiazem malate (USAN)|Diphenhydramine citrate (USP)|Dizocilpine maleate (USAN)|Dobutamine (USP/INN)|Dobutamine lactobionate (USAN)|Dobutamine tartrate (USP)|Donetidine (USAN)|Dopexamine (USAN/INN)|Dronedarone hydrochloride (USAN)|Ecopipam hydrochloride (USAN)|Edonentan (USAN)|Ephedrine sulfate (USP)|Erlotinib hydrochloride (JAN/USAN)|Lapatinib tosilate hydrate (JAN)|Mubritinib (USAN/INN)|Chlorpromazine phenolphthalinate (JAN)|Eprosartan (USAN/INN)|Esoxybutynin chloride (USAN)|Ethybenztropine (USAN)|Etintidine hydrochloride (USAN)|Eucatropine hydrochloride (USP XXXII)|Saralasin acetate (USAN)|Fenfluramine hydrochloride (USAN)|Fenobam (USAN)|Fenoterol (USAN/INN)|Fiduxosin hydrochloride (USAN)|Flestolol sulfate (USAN)|Flupirtine maleate (USAN)|Forasartan (USAN/INN)|Gavestinel (USAN/INN)|Hyoscyamine hydrobromide (USP)|Ibopamine (USAN/INN)|Icatibant acetate (USAN)|Icotidine (USAN)|Ifetroban (USAN/INN)|Ifetroban sodium (USAN)|Impromidine hydrochloride (USAN)|Indoramin (USAN/INN)|Indoramin hydrochloride (USAN)|Isoetharine (USP)|Isoetharine mesylate (USP)|Istradefylline (JAN/USAN/INN)|Lacidipine (USAN/INN)|Lavoltidine succinate (USAN)|Levalbuterol tartrate (USAN)|Levdobutamine lactobionate (USAN)|Levobetaxolol hydrochloride (USAN)|Lexipafant (USAN/INN)|Licostinel (USAN/INN)|Lubazodone hydrochloride (USAN)|Lupitidine hydrochloride (USAN)|Lurasidone hydrochloride (JAN/USAN)|Lutropin alfa (USAN/INN)|Maropitant citrate (USAN)|Medroxalol (USAN/INN)|Medroxalol hydrochloride (USAN)|Memantine hydrochloride (JAN/USAN)|Metaproterenol polistirex (USAN)|Methacholine chloride (USAN/INN)|Metiamide (USAN/INN)|Metoclopramide hydrochloride (USAN)|Metoprolol fumarate (USP)|Metrenperone (USAN/INN)|Mibefradil dihydrochloride (USAN)|Midostaurin (USAN/INN)|Milameline hydrochloride (USAN)|Trimetoquinol hydrochloride hydrate (JP16)|Nebivolol (USAN/INN)|Neramexane mesylate (USAN)|Norepinephrine bitartrate (USP)|Olmesartan (USAN/INN)|Serum gonadotrophin (JP16)|Pirenzepine hydrochloride hydrate (JP16)|Formoterol fumarate hydrate (JP16)|Oxmetidine hydrochloride (USAN)|Oxmetidine mesylate (USAN)|Paliperidone (JAN/USAN/INN)|Paliperidone palmitate (JAN/USAN)|Pamatolol sulfate (USAN)|Panitumumab (genetical recombination) (JAN)|Procaterol hydrochloride hydrate (JP16)|Pazopanib hydrochloride (JAN/USAN)|Pelanserin hydrochloride (USAN)|Pelitinib (USAN/INN)|Aminophylline hydrate (JP16)|Pertuzumab (genetical recombination) (JAN)|Perzinfotel (USAN/INN)|Phencyclidine hydrochloride (USAN)|Piboserod hydrochloride (USAN)|Picumeterol fumarate (USAN)|Pilocarpine nitrate (USP)|Pizotyline (USAN)|Practolol (USAN)|Prenalterol hydrochloride (USAN)|Pseudoephedrine polistirex (USAN)|Pseudoephedrine sulfate (USP)|Ranitidine bismuth citrate (USAN)|Regadenoson (USAN/INN)|Remacemide hydrochloride (USAN)|Reproterol hydrochloride (USAN)|Ridogrel (USAN/INN)|Rimiterol hydrobromide (USAN)|Ritanserin (USAN/INN)|Salmeterol (USAN/INN)|Sibenadet hydrochloride (USAN)|Solabegron hydrochloride (USAN)|Sufotidine (USAN/INN)|Sulamserod hydrochloride (USAN)|Sulotroban (USAN/INN)|Talnetant hydrochloride (USAN)|Talsaclidine fumarate (USAN)|Tandutinib (USAN/INN)|Tegaserod (USAN/INN)|Thyrotropin alfa (genetical recombination) (JAN)|Tiotidine (USAN/INN)|Traxoprodil mesylate (USAN)|Tripelennamine citrate|Tropanserin hydrochloride (USAN)|Sorafenib tosilate (JAN)|Imidafenacin (JAN/INN)|Tafluprost (JAN/USAN/INN)|Vapiprost hydrochloride (JAN/USAN)|Vatalanib (USAN/INN)|Vofopitant dihydrochloride (USAN)|Xamoterol (USAN)|Xamoterol fumarate (USAN)|Xanomeline (USAN)|Xanomeline tartrate (USAN)|Zacopride hydrochloride (USAN)|Zaltidine hydrochloride (USAN)|Renzapride (INN)|Sunitinib malate (JAN/USAN)|Vandetanib (JAN/USAN/INN)|Nilotinib hydrochloride hydrate (JAN)|Dasatinib hydrate (JAN)|Chorionic gonadotrophin (JP16)|Purified human menopausal gonadotrophin (JAN)|Serum gonadotrophin for injection (JP16)|Alcaftadine (USAN/INN)|Casopitant mesylate (USAN)|Fosaprepitant meglumine (JAN)|Lorcaserin hydrochloride (USAN)|Nebivolol hydrochloride (USAN)|Olanzapine pamoate (USAN)|Epanolol (USAN/INN)|Terlipressin (USAN/INN)|Motesanib|Niperotidine (INN)|Ambrisentan (JAN/INN)|Cimetropium bromide (INN)|Alfuzosin (INN)|Alimemazine (INN)|Oxedrine (BAN)|Alprenolol (INN)|Mepindolol (INN)|Tertatolol (INN)|Cloranolol (INN)|Talinolol (INN)|Chlorphenoxamine (INN)|Metergoline (INN)|Ornipressin (INN)|Demoxytocin (INN)|Carbetocin (INN/BAN)|Esketamine (INN)|Choline alfoscerate (INN)|Bambuterol (INN)|Chlorphenamine (INN)|Levocetirizine (USAN/INN)|Pimethixene (INN)|Amantadine (INN)|Amlodipine (INN)|Amosulalol (INN)|Apomorphine (BAN)|Arformoterol (INN)|Arotinolol (INN)|Atosiban acetate|Atropine oxide (INN)|Azatadine (INN)|Azelastine (INN)|Bambuterol hydrocloride|Barnidipine (INN)|Benidipine (INN)|Benzatropine (INN)|Bepridil (INN)|Betaxolol (INN)|Bitolterol (INN)|Bopindolol (INN)|Bosentan (INN)|Brompheniramine (INN)|Bunazosin (INN)|Buphenine (INN)|Bupranolol (INN)|Carazolol (INN)|Carbinoxamine (INN)|Carteolol (INN)|Celiprolol (INN)|Cetirizine (INN)|Cevimeline (INN)|Clazosentan sodium (JAN)|Chlorphenoxamine hydrochloride|Clenbuterol (INN)|Cinnarizine dihydrochloride|Zibotentan (JAN/USAN/INN)|Conivaptan (INN)|Cyclopentolate (INN)|Cyproheptadine (INN)|Dexchlorpheniramine (INN)|Dexfenfluramine (INN)|Dicycloverine (INN)|Dihydroergotamine (INN)|Dihydroergotamine tartrate|Diltiazem (INN)|Dimetindene (INN)|Dimetotiazine (INN)|Dioxopromethazine hydrochloride|Diphenylpyraline (INN)|Dopamine (INN)|Doxazosin (INN)|Doxylamine (INN)|Efonidipine (INN)|Emedastine (INN)|Epinastine (INN)|Ergometrine (INN)|Ergotamine (INN)|Erlotinib (INN)|Esmolol (INN)|Etilefrine (INN)|Fentonium bromide (INN)|Fexofenadine (INN)|Flunarizine (INN)|Flupentixol decanoate|Formoterol (INN)|Gallopamil (INN)|Hexoprenaline (INN)|Histamine (DCF)|Homochlorcyclizine (INN)|Hydroxyzine (INN)|Ibopamine hydrochloride|Ifenprodil (INN)|Imatinib (INN)|Azilsartan medoxomil (USAN)|Penbutolol (INN)|Isoprenaline (INN)|Isothipendyl (INN)|Isoxsuprine (INN)|Isoxsuprine lactate|Ketamine (INN)|Ketanserin tartrate|Ketotifen (INN)|Labetalol (INN)|Lapatinib (INN)|Levobunolol (INN)|Levocetirizine hydrochloride (JAN/USAN)|Levomethadone (INN)|Levomethadone hydrochloride|Levosalbutamol (INN)|Losartan (INN)|Manidipine (INN)|Mazaticol (INN)|Memantine (INN)|Mepyramine (INN)|Mepyramine theophyllineacetate|Metaraminol (INN)|Methadone (BAN)|Methylephedrine (BAN)|Methylergometrine (INN)|Mianserin (INN)|Mibefradil (INN)|Midodrine (INN)|Montelukast (INN)|Mosapramine (INN)|Mosapride (INN)|Moxisylyte (INN)|Naphazoline (INN)|Nicardipine (INN)|Norepinephrine hydrochoride|Norfenefrine (INN)|Olopatadine (INN)|Orciprenaline (INN)|Orphenadrine (INN)|Oxedrine tartrate|Oxedrine hydrochloride|Oxprenolol (INN)|Oxymetazoline (INN)|Oxyphencyclimine (INN)|Phenindamine (INN)|Pheniramine (INN)|Phenoxybenzamine (INN)|Phentolamine (INN)|Phenylephrine (INN)|Phenylephrine tartrate|Pilocarpine borate|Piperidolate (INN)|Pipethanate (INN)|Pirbuterol (INN)|Pirenzepine (INN)|Piroheptine (INN)|Pizotifen malate|Pranlukast (INN)|Prazosin (INN)|Procaterol (INN)|Procyclidine (INN)|Profenamine (INN)|Promethazine maleate|Propiverine (INN)|Propranolol (INN)|Pseudoephedrine (INN)|Quetiapine (INN)|Reproterol (INN)|Roxatidine (INN)|Roxatidine acetate (BAN)|Sarpogrelate (INN)|Setiptiline (INN)|Solifenacin (INN)|Sorafenib (USAN/INN)|Sotalol (INN)|Sunitinib (INN)|Tamsulosin (INN)|Terazosin (INN)|Terbutaline (INN)|Terlipressin acetate (JAN)|Tertatolol hydrochloride|Tetryzoline (INN)|Tiemonium methylsulfate|Timolol (INN)|Tolazoline (INN)|Tramazoline (INN)|Tretoquinol (INN)|Trihexyphenidyl (INN)|Trimebutine (INN)|Tripelennamine (INN)|Triprolidine (INN)|Ulobetasol (INN)|Unoprostone (INN)|Urapidil hydrochloride|Calcium valproate|Ziprasidone (INN)|Zuclopenthixol acetate|Zuclopenthixol decanoate|Zuclopenthixol dihydrochloride|Promethazine hibenzate|Azilsartan (JAN/USAN/INN)|Motesanib diphosphate (USAN)|Neratinib (INN/USAN)|Nilotinib (USAN/INN)|Phenylephrine bitartrate (USP)|Prucalopride (USAN/INN)|Indacaterol (USAN/INN)|Indacaterol maleate (JAN/USAN)|Mirabegron (USAN/JAN)|Afatinib (USAN/INN)|Ritobegron ethyl hydrochloride (JAN)|Afatinib maleate (JAN)|Carpronium chloride hydrate (JAN)|Norepinephrine hydrochloride (JAN)|Montirelin hydrate (JAN)|Lenvatinib (USAN/INN)|Lenvatinib mesylate (USAN)|Vipadenant (USAN/INN)|Eplivanserin (USAN/INN)|Olodaterol hydrochloride (JAN/USAN)|Zalutumumab (USAN/INN)|Cabozantinib (USAN)|Crenolanib (USAN)|Crenolanib besylate (USAN)|Regorafenib (USAN/INN)	Ca2+ that enters the cell from the outside is a principal source of signal Ca2+. Entry of Ca2+ is driven by the presence of a large electrochemical gradient across the plasma membrane. Cells use this external source of signal Ca2+ by activating various entry channels with widely different properties. The voltage-operated channels (VOCs) are found in excitable cells and generate the rapid Ca2+ fluxes that control fast cellular processes. There are many other Ca2+-entry channels, such as the receptor-operated channels (ROCs), for example the NMDA (N-methyl-D-aspartate) receptors (NMDARs) that respond to glutamate. There also are second-messenger-operated channels (SMOCs) and store-operated channels (SOCs).|The other principal source of Ca2+ for signalling is the internal stores that are located primarily in the endoplasmic/sarcoplasmic reticulum (ER/SR), in which inositol-1,4,5-trisphosphate receptors (IP3Rs) or ryanodine receptors (RYRs) regulate the release of Ca2+. The principal activator of these channels is Ca2+ itself and this process of Ca2+-induced Ca2+ release is central to the mechanism of Ca2+ signalling. Various second messengers or modulators also control the release of Ca2+. IP3, which is generated by pathways using different isoforms of phospholipase C (PLCbeta, delta, epsilon, gamma and zeta), regulates the IP3Rs. Cyclic ADP-ribose (cADPR) releases Ca2+ via RYRs. Nicotinic acid adenine dinucleotide phosphate (NAADP) may activate a distinct Ca2+ release mechanism on separate acidic Ca2+ stores. Ca2+ release via the NAADP-sensitive mechanism may also feedback onto either RYRs or IP3Rs. cADPR and NAADP are generated by CD38. This enzyme might be sensitive to the cellular metabolism, as ATP and NADH inhibit it.|The influx of Ca2+ from the environment or release from internal stores causes a very rapid and dramatic increase in cytoplasmic calcium concentration, which has been widely exploited for signal transduction. Some proteins, such as troponin C (TnC) involved in muscle contraction, directly bind to and sense Ca2+. However, in other cases Ca2+ is sensed through intermediate calcium sensors such as calmodulin (CALM).
hsa05160	Hepatitis C - Homo sapiens (human)	Human Diseases; Infectious Diseases	3949:LDLR|949:SCARB1|975:CD81|9080:CLDN9|7122:CLDN5|9071:CLDN10|9075:CLDN2|1365:CLDN3|9074:CLDN6|9073:CLDN8|5010:CLDN11|23562:CLDN14|9076:CLDN1|24146:CLDN15|26285:CLDN17|53842:CLDN22|10686:CLDN16|49861:CLDN20|149461:CLDN19|137075:CLDN23|1366:CLDN7|1364:CLDN4|51208:CLDN18|100506658:OCLN|4938:OAS1|4940:OAS3|4939:OAS2|6041:RNASEL|23586:DDX58|57506:MAVS|7187:TRAF3|29110:TBK1|9641:IKBKE|3661:IRF3|3665:IRF7|3456:IFNB1|7098:TLR3|148022:TICAM1|7189:TRAF6|8737:RIPK1|1147:CHUK|3551:IKBKB|8517:IKBKG|4792:NFKBIA|4790:NFKB1|5970:RELA|5610:EIF2AK2|27102:EIF2AK1|440275:EIF2AK4|9451:EIF2AK3|3659:IRF1|1965:EIF2S1|3576:IL8|6774:STAT3|3434:IFIT1|439996:IFIT1B|3646:EIF3E|3449:IFNA16|3447:IFNA13|3444:IFNA7|3443:IFNA6|3451:IFNA17|3442:IFNA5|3445:IFNA8|3441:IFNA4|3446:IFNA10|3448:IFNA14|3452:IFNA21|3440:IFNA2|3439:IFNA1|3454:IFNAR1|3455:IFNAR2|3716:JAK1|7297:TYK2|6772:STAT1|6773:STAT2|10379:IRF9|9021:SOCS3|5518:PPP2R1A|5519:PPP2R1B|55844:PPP2R2D|5520:PPP2R2A|5522:PPP2R2C|5521:PPP2R2B|5516:PPP2CB|5515:PPP2CA|8554:PIAS1|51588:PIAS4|10401:PIAS3|9063:PIAS2|1950:EGF|1956:EGFR|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|673:BRAF|5894:RAF1|369:ARAF|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|5602:MAPK10|5601:MAPK9|5599:MAPK8|5594:MAPK1|5595:MAPK3|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|5163:PDK1|207:AKT1|208:AKT2|10000:AKT3|2932:GSK3B|572:BAD|7157:TP53|1026:CDKN1A|7124:TNF|7132:TNFRSF1A|7186:TRAF2|8717:TRADD|10197:PSME3|6256:RXRA|5465:PPARA|10062:NR1H3	Hepatitis C	Interferon alfa-2a (genetical recombination) (JAN)|Interferon beta (JAN)	Hepatitis C virus (HCV) is a major cause of chronic liver disease. The HCV employ several strategies to perturb host cell immunity. After invasion, HCV RNA genome functions directly as an mRNA in the cytoplasm of the host cell and forms membrane-associated replication complexes along with non-structural proteins. Viral RNA can trigger the RIG-I pathway and interferon production during this process. Translated HCV protein products regulate immune response to inhibit the action of interferon. HCV core and NS5A proteins appear to be the most important molecules with regulatory functions that modulate transcription, cellular proliferation, and apoptosis.
hsa04916	Melanogenesis - Homo sapiens (human)	Organismal Systems; Endocrine System	5443:POMC|434:ASIP|4157:MC1R|2778:GNAS|107:ADCY1|108:ADCY2|109:ADCY3|196883:ADCY4|111:ADCY5|112:ADCY6|113:ADCY7|114:ADCY8|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|1385:CREB1|10488:CREB3|64764:CREB3L2|84699:CREB3L3|148327:CREB3L4|90993:CREB3L1|1387:CREBBP|2033:EP300|4286:MITF|7471:WNT1|7482:WNT2B|7472:WNT2|7473:WNT3|89780:WNT3A|54361:WNT4|7474:WNT5A|81029:WNT5B|7475:WNT6|7477:WNT7B|7476:WNT7A|7479:WNT8B|7478:WNT8A|7483:WNT9A|7484:WNT9B|7480:WNT10B|80326:WNT10A|7481:WNT11|51384:WNT16|8321:FZD1|8324:FZD7|2535:FZD2|7976:FZD3|8322:FZD4|8325:FZD8|7855:FZD5|8323:FZD6|8326:FZD9|11211:FZD10|2775:GNAO1|2776:GNAQ|1856:DVL2|1857:DVL3|1855:DVL1|2932:GSK3B|1499:CTNNB1|6932:TCF7|83439:TCF7L1|6934:TCF7L2|51176:LEF1|4254:KITLG|3815:KIT|3265:HRAS|3845:KRAS|4893:NRAS|5894:RAF1|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|7299:TYR|7306:TYRP1|1638:DCT|1910:EDNRB|2773:GNAI3|2770:GNAI1|2771:GNAI2|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|5579:PRKCB|5578:PRKCA|5582:PRKCG|1906:EDN1	Oculocutaneous albinism (OCA)|Ocular albinism|Piebaldism|Odontoonychodermal dysplasia|Waardenburg syndrome (WS)|Waardenburg syndrome (WS)|ABCD syndrome|Familial progressive hyperpigmentation|Pilomatricoma|Tietz syndrome	Corticotropin (USP/INN)|Cosyntropin (USAN)|Bosentan hydrate (JAN)|Tetracosactide acetate (JAN)|Corticotropin zinc hydroxide (USP)|Corticotropin, repository (USP)|Bosentan (INN)	Cutaneous melanin pigment plays a critical role in camouflage, mimicry, social communication, and protection against harmful effects of solar radiation. Melanogenesis is under complex regulatory control by multiple agents. The most important positive regulator of melanogenesis is the MC1 receptor with its ligands melanocortic peptides. MC1R activates the cyclic AMP (cAMP) response-element binding protein (CREB). Increased expression of MITF and its activation by phosphorylation (P) stimulate the transcription of tyrosinase (TYR), tyrosinase-related protein 1 (TYRP1), and dopachrome tautomerase (DCT), which produce melanin. Melanin synthesis takes place within specialized intracellular organelles named melanosomes. Melanin-containing melanosomes then move from the perinuclear region to the dendrite tips and are transferred to keratinocytes by a still not well-characterized mechanism.
hsa00100	Steroid biosynthesis - Homo sapiens (human)	Metabolism; Lipid Metabolism	4047:LSS|1595:CYP51A1|7108:TM7SF2|10826:C5orf4|6307:MSMO1|50814:NSDHL|51478:HSD17B7|10682:EBP|1718:DHCR24|6309:SC5DL|1717:DHCR7|3988:LIPA|1056:CEL|6646:SOAT1|8435:SOAT2|120227:CYP2R1|1594:CYP27B1|1591:CYP24A1	Lysosomal acid lipase deficiency|Smith-Lemli-Opitz syndrome|Congenital hemidysplasia with ichthyosiform nevus and limb defects (CHILD)|Desmosterolosis|Vitamin D-dependent rickets|X-linked chondrodysplasia punctata		
hsa00980	Metabolism of xenobiotics by cytochrome P450 - Homo sapiens (human)	Metabolism; Xenobiotics Biodegradation and Metabolism	1543:CYP1A1|1544:CYP1A2|1545:CYP1B1|1549:CYP2A7|1548:CYP2A6|1553:CYP2A13|1555:CYP2B6|1562:CYP2C18|1559:CYP2C9|1557:CYP2C19|1558:CYP2C8|1565:CYP2D6|1571:CYP2E1|1572:CYP2F1|29785:CYP2S1|1551:CYP3A7|1577:CYP3A5|64816:CYP3A43|1576:CYP3A4|4257:MGST1|4258:MGST2|2940:GSTA3|2939:GSTA2|2946:GSTM2|2941:GSTA4|2948:GSTM4|2953:GSTT2|2949:GSTM5|2947:GSTM3|9446:GSTO1|4259:MGST3|119391:GSTO2|2938:GSTA1|2952:GSTT1|2944:GSTM1|2950:GSTP1|221357:GSTA5|373156:GSTK1|2052:EPHX1|6822:SULT2A1|1109:AKR1C4|8644:AKR1C3|1646:AKR1C2|1645:AKR1C1|27294:DHDH|873:CBR1|874:CBR3|8574:AKR7A2|22977:AKR7A3|222:ALDH3B2|220:ALDH1A3|221:ALDH3B1|218:ALDH3A1|126:ADH1C|131:ADH7|124:ADH1A|125:ADH1B|127:ADH4|128:ADH5|130:ADH6|7363:UGT2B4|574537:UGT2A2|7367:UGT2B17|7365:UGT2B10|7364:UGT2B7|7366:UGT2B15|54577:UGT1A7|10720:UGT2B11|54490:UGT2B28|54579:UGT1A5|54659:UGT1A3|54657:UGT1A4|54578:UGT1A6|54576:UGT1A8|54600:UGT1A9|10941:UGT2A1|54575:UGT1A10|79799:UGT2A3|54658:UGT1A1|3290:HSD11B1	Peters anomaly|Cortisone reductase deficiency (CRD)|Primary congenital glaucoma (PCG)	Fomepizole (USAN/INN)	
hsa04115	p53 signaling pathway - Homo sapiens (human)	Cellular Processes; Cell Growth and Death	472:ATM|11200:CHEK2|545:ATR|1111:CHEK1|1029:CDKN2A|4193:MDM2|4194:MDM4|7157:TP53|1026:CDKN1A|595:CCND1|894:CCND2|896:CCND3|1019:CDK4|1021:CDK6|9134:CCNE2|898:CCNE1|1017:CDK2|2810:SFN|56475:RPRM|9133:CCNB2|891:CCNB1|85417:CCNB3|983:CDK1|4616:GADD45B|1647:GADD45A|10912:GADD45G|51512:GTSE1|355:FAS|55367:PIDD|841:CASP8|637:BID|581:BAX|5366:PMAIP1|27113:BBC3|63970:TP53AIP1|9540:TP53I3|9538:EI24|51246:SHISA5|64065:PERP|64393:ZMAT3|6477:SIAH1|54205:CYCS|317:APAF1|842:CASP9|836:CASP3|3486:IGFBP3|3479:IGF1|5054:SERPINE1|575:BAI1|3732:CD82|5268:SERPINB5|1643:DDB2|6241:RRM2|50484:RRM2B|27244:SESN1|83667:SESN2|143686:SESN3|5728:PTEN|7249:TSC2|55240:STEAP3|64326:RFWD2|25898:RCHY1|900:CCNG1|901:CCNG2|8493:PPM1D|7161:TP73|7057:THBS1|8795:TNFRSF10B	Ataxia with ocular apraxia (AOA)|Li-Fraumeni syndrome|Lymphangioleiomyomatosis (LAM)|Tuberous sclerosis complex (TSC)|Seckel syndrome|Choroid plexus papilloma|Plasminogen activator inhibitor type 1 (PAI-1) deficiency|VACTERL/VATER association	Hydroxycarbamide (JAN/INN)	p53 activation is induced by a number of stress signals, including DNA damage, oxidative stress and activated oncogenes. The p53 protein is employed as a transcriptional activator of p53-regulated genes. This results in three major outputs; cell cycle arrest, cellular senescence or apoptosis. Other p53-regulated gene functions communicate with adjacent cells, repair the damaged DNA or set up positive and negative feedback loops that enhance or attenuate the functions of the p53 protein and integrate these stress responses with other signal transduction pathways.
hsa04961	Endocrine and other factor-regulated calcium reabsorption - Homo sapiens (human)	Organismal Systems; Excretory System	5745:PTH1R|2778:GNAS|112:ADCY6|115:ADCY9|5613:PRKX|5568:PRKACG|5566:PRKACA|5567:PRKACB|7421:VDR|2099:ESR1|56302:TRPV5|9365:KL|26052:DNM3|1785:DNM2|10059:DNM1L|1759:DNM1|161:AP2A2|160:AP2A1|163:AP2B1|1173:AP2M1|1175:AP2S1|1211:CLTA|1212:CLTB|8218:CLTCL1|1213:CLTC|8766:RAB11A|793:CALB1|476:ATP1A1|480:ATP1A4|478:ATP1A3|477:ATP1A2|481:ATP1B1|482:ATP1B2|483:ATP1B3|23439:ATP1B4|486:FXYD2|3816:KLK1|3817:KLK2|624:BDKRB2|2776:GNAQ|5331:PLCB3|5332:PLCB4|5330:PLCB2|23236:PLCB1|5579:PRKCB|5578:PRKCA|5582:PRKCG|490:ATP2B1|6546:SLC8A1	Primary failure of tooth eruption|Centronuclear myopathy|Localized autosomal recessive hypotrichosis|Alternating hemiplegia of childhood|Vitamin D-dependent rickets|Familial tumoral calcinosis (FTC)	Estrone (JAN/USP/INN)|Estradiol (JAN/USP/INN)|Teriparatide acetate (JAN)|Deltibant (USAN/INN)|Parathyroid hormone (human) (USAN)|Teriparatide (genetical recombination) (JAN)|Teriparatide acetate (USAN)|Fispemifene (USAN/INN)	Calcium (Ca2+) is essential for numerous physiological functions including intracellular signalling processes, neuronal excitability, muscle contraction and bone formation. Therefore, its homeostasis is finely maintained through the coordination of intestinal absorption, renal reabsorption, and bone resorption. In kidney, the late part of the distal convoluted tubule (DCT) and the connecting tubule (CNT) are the site of active Ca2+ transport and precisely regulate Ca2+ reabsorption. Following Ca2+ entry through TRPV5, Ca2+ bound to calbindin-D28K diffuses to the basolateral side, where it is extruded into the blood compartment through NCX1 and to a lesser extent PMCA1b. In the urinary compartment, both klotho and tissue kallikrein (TK) increase the apical abundance of TRPV5. In the blood compartment, PTH, 1,25(OH)2D3 and estrogen increase the transcription and protein expression of  the luminal Ca2+ channels, calbindins, and the extrusion systems.
hsa04722	Neurotrophin signaling pathway - Homo sapiens (human)	Organismal Systems; Nervous System	4803:NGF|627:BDNF|4909:NTF4|4908:NTF3|4914:NTRK1|4915:NTRK2|4916:NTRK3|10603:SH2B2|10019:SH2B3|25970:SH2B1|2885:GRB2|6654:SOS1|6655:SOS2|3265:HRAS|3845:KRAS|4893:NRAS|5894:RAF1|673:BRAF|5604:MAP2K1|5605:MAP2K2|5594:MAPK1|5595:MAPK3|6195:RPS6KA1|6196:RPS6KA2|6197:RPS6KA3|27330:RPS6KA6|9252:RPS6KA5|8986:RPS6KA4|468:ATF4|596:BCL2|57498:KIDINS220|10818:FRS2|1399:CRKL|1398:CRK|2889:RAPGEF1|5906:RAP1A|5908:RAP1B|4215:MAP3K3|5607:MAP2K5|5598:MAPK7|5603:MAPK13|5600:MAPK11|6300:MAPK12|1432:MAPK14|9261:MAPKAPK2|25759:SHC2|6464:SHC1|53358:SHC3|399694:SHC4|2549:GAB1|8503:PIK3R3|23533:PIK3R5|5296:PIK3R2|5295:PIK3R1|5293:PIK3CD|5291:PIK3CB|5294:PIK3CG|5290:PIK3CA|207:AKT1|208:AKT2|10000:AKT3|4793:NFKBIB|4792:NFKBIA|4794:NFKBIE|4790:NFKB1|5970:RELA|2309:FOXO3|356:FASLG|572:BAD|2932:GSK3B|5163:PDK1|8471:IRS4|8660:IRS2|3667:IRS1|5335:PLCG1|5336:PLCG2|810:CALML3|163688:CALML6|808:CALM3|805:CALM2|801:CALM1|51806:CALML5|815:CAMK2A|816:CAMK2B|817:CAMK2D|818:CAMK2G|814:CAMK4|25:ABL1|5781:PTPN11|4145:MATK|4804:NGFR|397:ARHGDIB|396:ARHGDIA|387:RHOA|998:CDC42|5879:RAC1|4214:MAP3K1|4217:MAP3K5|5609:MAP2K7|5602:MAPK10|5601:MAPK9|5599:MAPK8|3725:JUN|7157:TP53|581:BAX|7161:TP73|7189:TRAF6|10782:ZNF274|11108:PRDM4|9500:MAGED1|27018:NGFRAP1|7529:YWHAB|7532:YWHAG|7533:YWHAH|10971:YWHAQ|7534:YWHAZ|7531:YWHAE|8767:RIPK2|3654:IRAK1|3656:IRAK2|11213:IRAK3|51135:IRAK4|3551:IKBKB|6272:SORT1|5663:PSEN1|5664:PSEN2|5580:PRKCD	Frontotemporal lobar degeneration (FTLD)|Type I diabetes mellitus|Acne inversa|Congenital central hypoventilation syndrome (CCHS)|Choroid plexus papilloma|Metachondromatosis	Begacestat (USAN/INN)|Tarenflurbil (INN/USAN)|Semagacestat (USAN/INN)|Avagacestat (USAN)	Neurotrophins are a family of trophic factors involved in differentiation and survival of neural cells. The neurotrophin family consists of nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), and neurotrophin 4 (NT-4). Neurotrophins exert their functions through engagement of Trk tyrosine kinase receptors or p75 neurotrophin receptor (p75NTR). Neurotrophin/Trk signaling is regulated by connecting a variety of intracellular signaling cascades, which include MAPK pathway, PI-3 kinase pathway, and PLC pathway, transmitting positive signals like enhanced survival and growth. On the other hand, p75NTR transmits both positive and nagative signals. These signals play an important role for neural development and additional higher-order activities such as learning and memory.
hsa00561	Glycerolipid metabolism - Homo sapiens (human)	Metabolism; Lipid Metabolism	132158:GLYCTK|219:ALDH1B1|224:ALDH3A2|217:ALDH2|501:ALDH7A1|223:ALDH9A1|231:AKR1B1|10327:AKR1A1|26007:DAK|2712:GK2|2710:GK|150763:GPAT2|57678:GPAM|137964:AGPAT6|84803:AGPAT9|10554:AGPAT1|10555:AGPAT2|253558:LCLAT1|129642:MBOAT2|154141:MBOAT1|56895:AGPAT4|56894:AGPAT3|8611:PPAP2A|8613:PPAP2B|8612:PPAP2C|8525:DGKZ|1607:DGKB|1609:DGKQ|1608:DGKG|9162:DGKI|8527:DGKD|1606:DGKA|8526:DGKE|160851:DGKH|8694:DGAT1|84649:DGAT2|346606:MOGAT3|9388:LIPG|3990:LIPC|1056:CEL|80339:PNPLA3|5406:PNLIP|5407:PNLIPRP1|5408:PNLIPRP2|119548:PNLIPRP3|8513:LIPF|4023:LPL|55750:AGK|11343:MGLL|2717:GLA|23175:LPIN1|57016:AKR1B10|64900:LPIN3|9663:LPIN2	Hyperlipoproteinemia, type I|Glycerol kinase deficiency (GKD)|Majeed syndrome	Cyanamide (JP16)|Disulfiram (JP16/USP/INN)|Ibrolipim (USAN/INN)	
hsa00860	Porphyrin and chlorophyll metabolism - Homo sapiens (human)	Metabolism; Metabolism of Cofactors and Vitamins	211:ALAS1|212:ALAS2|124454:EARS2|2058:EPRS|210:ALAD|3145:HMBS|7390:UROS|7389:UROD|1371:CPOX|5498:PPOX|2235:FECH|1352:COX10|1355:COX15|326625:MMAB|3162:HMOX1|3163:HMOX2|644:BLVRA|645:BLVRB|7363:UGT2B4|574537:UGT2A2|7367:UGT2B17|7365:UGT2B10|7364:UGT2B7|7366:UGT2B15|54577:UGT1A7|10720:UGT2B11|54490:UGT2B28|54579:UGT1A5|54659:UGT1A3|54657:UGT1A4|54578:UGT1A6|54576:UGT1A8|54600:UGT1A9|10941:UGT2A1|54575:UGT1A10|79799:UGT2A3|54658:UGT1A1|2990:GUSB|3052:HCCS|1356:CP|94033:FTMT|2495:FTH1|2512:FTL	Erythropoietic porphyria (EP)|Hepatic porphyria|Hyperbilirubinemia|Neurodegeneration with brain iron accumulation (NBIA)|Anophthalmia and microphthalmia (A/M)