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Fig. 3 | BMC Systems Biology

Fig. 3

From: Dynamic Optimization with Particle Swarms (DOPS): a meta-heuristic for parameter estimation in biochemical models

Fig. 3

Schematic of the extrinsic and intrinsic coagulation cascade. Inactive zymogens upstream (grey) are activated by exposure to tissue factor (TF) following vessel injury. Tissue factor and activated factor VIIa (FVIIa) form a complex that activates factor X (fX) and IX (fIX). FXa activates downstream factors including factor VIII (fVIII) and fIX. Factor V (fV) is primarily activated by thrombin (FIIa). In addition, we included a secondary fV activation route involving FXa. FXa and FVa form a complex (prothrombinase) on activated platelets that converts prothrombin (fII) to FIIa. FIXa and FVIIIa can also form a complex (tenase) on activated platelets which catalyzes FXa formation. Thrombin also activates upstream coagulation factors, forming a strong positive feedback ensuring rapid activation. Tissue factor pathway inhibitor (TFPI) downregulates FXa formation and activity by sequestering free FXa and TF-FVIIa in a FXa-dependent manner. Antithrombin III (ATIII) inhibits all proteases. Thrombin inhibits itself binding the surface protein thrombomodulin (TM). The IIa-TM complex catalyzes the conversion of protein C (PC) to activated protein C (APC), which attenuates the coagulation response by the proteolytic cleavage of fV/FVa and fVIII/FVIIIa

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