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• W2908701659 abstract "Coagulation factor V (FV) is a large 330-kD glycoprotein mainly synthesized in the liver and megakaryocytes. Eighty percent of blood FV circulates in plasma while the remaining 20% is stored within platelet α granules.[1] In its active form (FVa), it is an essential cofactor for factor Xa, assisting the conversion of prothrombin to thrombin. The procoagulant activity of FVa is regulated by activated protein C (APC), which cleaves multiple peptide bonds in FVa. Cleavage of FV by APC at residue p.Arg534 (“Arg506” in legacy nomenclature) converts FV into an anticoagulant protein (FVac) that lacks procoagulant activity and serves as a cofactor to APC, which in synergy with protein S mediates degradation of FVIIIa.[1] FV is also a carrier of, and cofactor to, the coagulation inhibitor tissue factor pathway inhibitor.[2] [3] Defects in FV may therefore result in either hemorrhagic or thrombotic phenotypes. The FV Leiden mutation (“Arg506Gln” in legacy nomenclature; p.Arg534Gln in NM_000130.4) is the most common defect in FV leading to a thrombotic phenotype, while severe FV deficiency, an autosomal recessive condition due to point mutations in the FV gene (F5), can be associated with mild or severe bleeding.[4]" @default.
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• W2908701659 date "2019-01-10" @default.
• W2908701659 modified "2023-10-02" @default.
• W2908701659 title "Factor V Deficiency with a Thrombotic Clinical Phenotype" @default.
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• W2908701659 doi "https://doi.org/10.1055/s-0038-1677041" @default.
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