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• W982010 abstract "Tissue factor (TF) (CD 142) is the physiological initiator of normal coagulation and in many types of thrombosis. It is a transmembrane protein constitutively expressed on the surfaces of various cell types outside the vasculature, but not expressed on cells in contact with flowing blood. TF, a member of the cytokine receptor superfamily is a high affinity receptor for coagulation factor Vll/VIIa. It functions as an essential cofactor for factor VIIa to efficiently cleave its substrates, factor IX, and factor X, to their active forms. Increased TF activity has been implicated in a number of thrombotic conditions and hypercoagulable states. Increased expression of TF on the vascular endothelial cells (EC) and monocytes has been reported in the patients with cancer, gram-negative bacterial sepsis, atherosclerosis, and OKT3-induced coagulopathy in renal transplant patients. The protein C system plays a key role in normal hemostasis. Protein C, a vitamin K-dependent plasma glycoprotein, is the precursor of a serine protease. Protein C becomes activated when thrombin binds to thrombomodulin, a constitutively expressed protein on the surface of the vascular EC. On binding to thrombomodulin, thrombin's procoagulant activities are inhibited, and its ability to activate protein C is markedly enhanced. Activated protein C (APC) acts as an anticoagulant by proteolytically inactivating factors Va and VIIIa, thereby limiting the rate of thrombin generation. To efficiently inactivate factors Va and VIIIa, APC requires the cofactor activity of protein S, another vitamin K-dependent plasma glycoprotein. Protein S circulates in plasma in two forms, as a free protein and in a bimolecular complex with C4b-binding protein, a complement regulatory protein." @default.
• W982010 created "2016-06-24" @default.
• W982010 creator A5022325563 @default.
• W982010 date "2002-01-01" @default.
• W982010 modified "2023-09-27" @default.
• W982010 title "Tissue Factor, Protein C Pathway, and Other Hemostasis Abnormalities in the Pathogenesis of the Antiphospholipid Syndrome" @default.
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• W982010 doi "https://doi.org/10.1016/b978-044450987-1/50011-5" @default.
• W982010 hasPublicationYear "2002" @default.
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