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Therefore, although the coagulation cascade can be triggered in vitro through the intrinsic pathway only, in vivo coagulation is triggered by the extrinsic pathway. However, the model better describing how coagulation works is the so-called cell-based model, a more integrated picture of the whole process, in which phospholipid surfaces, such as ...
The division of coagulation in two pathways is arbitrary, originating from laboratory tests in which clotting times were measured either after the clotting was initiated by glass, the intrinsic pathway; or clotting was initiated by thromboplastin (a mix of tissue factor and phospholipids), the extrinsic pathway.
Traditional models of coagulation developed in the 1960s envisaged two separate cascades, the extrinsic (tissue factor (TF)) pathway and the intrinsic pathway. These pathways converge to a common point, the formation of the Factor Xa/Va complex which together with calcium and bound on a phospholipids surface, generate thrombin (Factor IIa) from ...
The kinin-kallikrein system plays a small role in coagulation. Blood clotting cascade. The blood clotting cascade consists of the intrinsic and extrinsic pathway, both of which create thrombin, a protease involved in blood clotting. The intrinsic pathway requires kininogen, specifically high molecular weight kininogen, as a cofactor.
HMWK is one of four proteins which interact to initiate the contact activation pathway (also called the intrinsic pathway) of coagulation: the other three are Factor XII, Factor XI and prekallikrein. HMWK is not enzymatically active, and functions only as a cofactor for the activation of kallikrein and factor XII. It is also necessary for the ...
[3] [4] Factor X can be activated by both the factor VIIa-tissue factor complex of the extrinsic coagulation pathway and by the tenase complex of the intrinsic pathway. The intrinsic tenase complex is composed of both factor IXa and factor VIIIa.
The two arms of the contact system. PKa's cleavage of HK liberates BK and promotes inflammation. FXIIa's cleavage of FXI initiates coagulation. In the contact activation system or CAS, three proteins in the blood, factor XII (FXII), prekallikrein (PK) and high molecular weight kininogen (HK), bind to a surface and cause blood coagulation and ...
Factor XI (FXI) is produced by the liver and circulates as a homo-dimer in its inactive form. [9] The plasma half-life of FXI is approximately 52 hours. The zymogen factor is activated into factor XIa by factor XIIa (FXIIa), thrombin, and FXIa itself; due to its activation by FXIIa, FXI is a member of the "contact pathway" (which includes HMWK, prekallikrein, factor XII, factor XI, and factor IX).