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F5 encodes an essential cofactor of the blood coagulation cascade. Additionally we are shipping Coagulation Factor V Kits (64) 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.
Double heterozygotes had a clinical presentation intermediate between FVL and prothrombin (show F2 Antibodies) mutation single carriers.
increased frequency of factor V Leiden G1691A and prothrombin (show F2 Antibodies) G20210A mutation in venous thromboembolism patients indicates a significant role of these mutations in the development of VTE in the Kashmiri population
genetic study of Factor V Leiden (G1691A) mutation in young ischemic strokes with large vessel disease in a South Indian population
the routine screening of patients with NAIS for F5 G1691A, F2 G20210A and MTHFR (show MTHFR Antibodies) C677T gene mutations might not be justified, and additional prothrombotic mechanisms should be considered.
There were no significant differences in factor V and factor II genotypes between infertile men and normal controls.
FVBonn induces hypercoagulability via a combination of increased activation/procoagulant activity, decreased susceptibility to Activated protein C (show PROC Antibodies)-mediated inactivation, and slightly reduced APC (show APC Antibodies) cofactor activity
prothrombotic mutations in factor V Leiden and prothrombin (show F2 Antibodies) as well as older age are risk factors for venous thrombosis
Heterozygous FV Leiden, homozygous PAI-1 4G/4G, heterozygous MTHFR C677T, homozygous MTHFR A1298C, as much as the combined thrombophilic genotypes MTHFR 677T + ACE Iota/D, MTHFR 677T/1298C + ACE D/D, ACE I/D + b-fibrinogen -455 G/A, FV HR2 + b-fibrinogen -455 G/A showed a correlation as risk factors for Recurrent pregnancy loss.
the signaling and anticoagulant functions of APC (show APC Antibodies) are in spatially and kinetically distinct compartments, and that it is possible to specifically inhibit the anticoagulant activity of APC (show APC Antibodies). Targeting APC (show APC Antibodies) with a serpin is remarkably effective and may be safe for long-term prophylactic use in the treatment of hemophilia.
Cleavage of FV at Arg(1545) , which abolishes the anticoagulant properties of FV and commits FV to the procoagulant pathway, is inhibited by binding of the TFPIalpha C-terminus to the FV acidic region
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