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F5 encodes an essential cofactor of the blood coagulation cascade. Additionally we are shipping Coagulation Factor V Antibodies (132) and Coagulation Factor V Kits (67) and many more products for this protein.
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Mice with the FVL mutation do not have increased spermatogenesis as compared to wildtype mice.
Platelet-derived FV contributes to the control of angiogenesis and is likely associated with thrombin (show F2 Proteins) generation in hind limb ischemia model.
These findings reveal a novel biological function and mechanism of the protein C (show PROC Proteins) pathway in which protein S and the aPC (show APC Proteins)-cleaved form of fV are cofactors for anti-inflammatory cell signaling by aPC (show APC Proteins) 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 Proteins) deficiency and FVL or other thrombosis-related gene defect in patients with genetic severe early-onset thrombosis.
Data suggest that tissue factor (show F3 Proteins) and factor V induction by LPS (show TLR4 Proteins) 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 Proteins) deficiency and Factor V Leiden toward tissue fibrin deposition; concomitant mutations in these genes may increase the penetrance of vascular thrombotic events in humans
factor V Leiden and MTHFR C677T polymorphisms were significantly associated with recurrent pregnancy loss (RPL) in Bosnian women...
the prothrombotic activity of FII is the result of a polymorphism and of a missense mutation, whereas that of FV derives only from a polymorphism. The observation that a clotting factor (show F7 Proteins) defect may be associated with both bleeding or venous thrombosis depending on the site of the mutation has caused an extensive reevaluation of the blood clotting mechanism.
study found the FVL A allele frequency and GA genotype are significantly more prevalent among patients with coronary artery disease (CAD) compared to controls and may be predisposing to CAD; further found that the FVL mutation is an independent risk factor whose effect is not modified by other risk factors; FV HR2 variation does not show any statistically significant association with CAD
suggesting that the FVL paradox is related to the carriership of one wild type and one mutated factor V allele
Review/Meta-analysis: Factor V G1691A single nucleotide gene polymorphism was associated with risk of ischemic stroke mainly in young adults.
Factor V Leiden mutation is associated with venous thromboembolism in cancer.
we were not able to confirm the association between the polymorphisms of f5, f2, and mthfr (show MTHFR Proteins) and pregnancy loss in Bosnian women
Human FVL carriers have a higher total sperm count than non-carriers, with an adjusted mean difference of 31 x 106 (95%CI 0.2-61.7; P = 0.048).
contribution of FVLeiden causing resistance to activated protein C in Indian population is not as strong as previously reported in Western countries
The frequencies of GA and AA genotypes and A allele of coagulation factor V (FV) 1691G>A polymorphism significantly increased in the lower extremity deep venous thrombosis (LDVT) group. Patients with LDVT carrying A allele (GA + AA) had both higher patency and recurrence rates than those carrying GG genotype. Coagulation factor V (FV) 1691G>A polymorphism may be associated with both the risk and prognosis of LDVT.
Data suggest factor Xa (FXa (show F10 Proteins)) and factor Va (FVa) compete to bind FXa (show F10 Proteins) on both PS model membranes and microparticles from activated platelets; this competition between dimerization/prothrombinase (show FGL2 Proteins) 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