Blood coagulation is a series of coordinated and calcium-dependent proenzyme-to-serine protease conversions likely to be localized on the surfaces of activated cells in vivo. It culminates in the formation of thrombin, the enzyme responsible for the conversion of soluble fibrinogen to the insoluble fibrin clot. 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. Complement is a system of plasma proteins that is activated by the presence of 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, intern, generates the effector molecules of complement. The three main consequences of complement activation are the opsonization of pathogens, the recruitment of inflammatory and immunocompetent cells, and the direct killing of pathogens. Source: KEGG Proteins on this pathway have targeted assays available via the [https://assays.cancer.gov/available_assays?wp_id=WP558 CPTAC Assay Portal] c93 CLU Type your comment here MGI:88235 LL:109828 map04610 KEGG Pathway https://www.genome.jp/dbget-bin/www_bget?pathway+map04610 complement system pathway PW:0000502 Pathway Ontology