作者: Clément Naudin , Elena Burillo , Stefan Blankenberg , Lynn Butler , Thomas Renné
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摘要: Contact activation is the surface-induced conversion of factor XII (FXII) zymogen to serine protease FXIIa. Blood-circulating FXII binds negatively charged surfaces and this contact triggers a conformational change in inducing autoactivation. Several that have capacity for initiating been identified, including misfolded protein aggregates, collagen, nucleic acids, platelet microbial polyphosphate. Activated initiates proinflammatory kallikrein-kinin system intrinsic coagulation pathway, leading formation bradykinin thrombin, respectively. well characterized vitro provides mechanistic basis diagnostic clotting assay, activated partial thromboplastin time. However, only past decade has critical role pathological thrombosis appreciated. While defective thromboprotection, excess underlies swelling disorder hereditary angioedema type III. This review an overview molecular activation–associated disease states.