The formation of a fibrin clot at the site of an injury to the wall of a normal blood vessel is an essential part of the process to stop blood loss after vascular injury. The reactions that lead to fibrin clot formation are commonly described as a cascade, in which the product of each step is an enzyme or cofactor needed for following reactions to proceed efficiently. The entire clotting cascade can be divided into three portions, the extrinsic pathway, the intrinsic pathway, and the common pathway. The extrinsic pathway begins with the release of tissue factor at the site of vascular injury and leads to the activation of factor X. The intrinsic pathway provides an alternative mechanism for activation of factor X, starting from the activation of factor XII. The common pathway consists of the steps linking the activation of factor X to the formation of a multimeric, cross-linked fibrin clot. Each of these pathways includes not only a cascade of events that generate the catalytic activities needed for clot formation, but also numerous positive and negative regulatory events

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A2M , SERPINC1 , C1QBP , SERPING1 , F2 , F2R , F3 , F5 , F7 , F8 , F9 , F10 , F11 , F12 , F13A1 , F13B , FGA , FGB , FGG , GP1BA , GP1BB , GP5 , GP9 , SERPIND1 , KLKB1 , KNG1 , SERPINA5 , PF4 , PF4V1 , SERPINE2 , PRCP , PROC , PROS1 , PRTN3 , TFPI , THBD , VWF , PROCR , CD177 ,