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F5 encodes an essential cofactor of the blood coagulation cascade. Additionally we are shipping Coagulation Factor V Kits (48) and Coagulation Factor V Proteins (23) and many more products for this protein.
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Platelet-derived FV contributes to the control of angiogenesis and is likely associated with thrombin (show F2 Antibodies) generation in hind limb ischemia model.
These findings reveal a novel biological function and mechanism of the protein C (show PROC Antibodies) pathway in which protein S and the aPC (show APC Antibodies)-cleaved form of fV are cofactors for anti-inflammatory cell signaling by aPC (show APC Antibodies) in the context of endotoxemia and infection
Mice deficient in LMAN1 exhibit FV and FVIII deficiencies and liver accumulation of alpha1-antitrypsin.
The FVL mutation does not influence coagulation activation, lung inflammation or survival in lethal influenza A.
It suggested that there could be a combination of GLA (show GLA Antibodies) deficiency and FVL or other thrombosis-related gene defect in patients with genetic severe early-onset thrombosis.
Data suggest that tissue factor (show F3 Antibodies) and factor V induction by LPS (show TLR4 Antibodies) may in part accelerate mesangioproliferative glomerulonephritis through activation of factor X and downstream proinflammatory and procoagulant mechanisms.
The source of the FVL leading to accelerated thrombosis appears to be circulating, non-platelet-derived plasma FVL.
FVL has the ability to improve the hemophilia A or B phenotype, but this effect is principally evident at the microcirculation level following a particular vascular injury.
observations demonstrate a synergistic interaction between alpha-galactosidase A (show GLA Antibodies) deficiency and Factor V Leiden toward tissue fibrin deposition; concomitant mutations in these genes may increase the penetrance of vascular thrombotic events in humans
Fetal gene defects precipitate platelet-mediated pregnancy failure in factor V Leiden mothers.
there is a synergistic effect of the FVL and rs4524 single nucleotide polymorphisms and active cancer on the risk of VTE.
Our finding that the C2-domain of FVIII (show F8 Antibodies) can be replaced by that of FV without compromising FVIII (show F8 Antibodies) activity may have translational implications.
These results demonstrate a new anticoagulant (cofactor) function of FV that targets the early phase of coagulation before prothrombinase (show F10 Antibodies) assembly
There was an increased odds of stillbirth for maternal homozygous factor V Leiden mutation.
Factor V Leiden was not associated with recurrent miscarriage during the first trimester of pregnancy in Brazilian women.
The prevalence of factor V G1691A, prothrombin (show F2 Antibodies) G20210A and MTHFR (show MTHFR Antibodies) C677T single nucleotide polymorphism among Syrians is 11.5%, 2.5% and 84.5%, respectively.
Desmopressin acetate has no effect on FV plasma concentration in patients with combined deficiency of factors V and VIII (show COX8A Antibodies).
F5 rs6025 and F11 (show F11 Antibodies) rs2289252 contributed to the risk of recurrent venous thromboembolism and the combination is of potential clinical relevance for risk prediction
Data does not support a role for factor V Leiden and G20210A prothrombin (show F2 Antibodies) gene mutations in the susceptibility to infective endocarditis.
Factor V (F5) c.1691G>A (Leiden) was present in 0.5% of 400 ischemic stroke patients in Sri (show SRI Antibodies) Lanka. F5 mutation was present in a statistically significant number of patients with venous thrombosis (P = .005) compared to those with arterial thrombosis.
Data suggest factor Xa (FXa (show F10 Antibodies)) and factor Va (FVa) compete to bind FXa (show F10 Antibodies) on both PS model membranes and microparticles from activated platelets; this competition between dimerization/prothrombinase (show FGL2 Antibodies) complex formation appears to regulate blood coagulation.
This gene encodes an essential cofactor of the blood coagulation cascade. This factor circulates in plasma, and is converted to the active form by the release of the activation peptide by thrombin during coagulation. This generates a heavy chain and a light chain which are held together by calcium ions. The activated protein is a cofactor that participates with activated coagulation factor X to activate prothrombin to thrombin. Defects in this gene result in either an autosomal recessive hemorrhagic diathesis or an autosomal dominant form of thrombophilia, which is known as activated protein C resistance.
coagulation factor V
, activated protein C cofactor
, activated protein c cofactor
, coagulation factor V jinjiang A2 domain
, factor V Leiden
, proaccelerin, labile factor