Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
F5 encodes an essential cofactor of the blood coagulation cascade.
Showing 10 out of 64 products:
Mouse (Murine) Coagulation Factor V ELISA Kit for Sandwich ELISA - ABIN415764
Wang, Braun, Zhang, Norström, Thorlacius: Thrombin generation in abdominal sepsis is Rho-kinase-dependent. in Biochemical and biophysical research communications 2015
Show all 2 Pubmed References
Mouse (Murine) Coagulation Factor V ELISA Kit for Sandwich ELISA - ABIN832489
Schlegel, Lesurtel, Melloul, Limani, Tschuor, Graf, Humar, Clavien: ALPPS: from human to mice highlighting accelerated and novel mechanisms of liver regeneration. in Annals of surgery 2014
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 ELISA Kits) generation in hind limb ischemia model.
These findings reveal a novel biological function and mechanism of the protein C (show PROC ELISA Kits) pathway in which protein S and the aPC (show APC ELISA Kits)-cleaved form of fV are cofactors for anti-inflammatory cell signaling by aPC (show APC ELISA Kits) 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 ELISA Kits) deficiency and FVL or other thrombosis-related gene defect in patients with genetic severe early-onset thrombosis.
Data suggest that tissue factor and factor V induction by LPS 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 ELISA Kits) deficiency and Factor V Leiden toward tissue fibrin deposition; concomitant mutations in these genes may increase the penetrance of vascular thrombotic events in humans
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 (show PROC ELISA Kits) 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.
Factor V Leiden-mutations were found in 16.8% of patients with cerebral sinus venous thrombosis and in 17.8% of patients with arterial ischemic stroke, which was significantly more frequent than in controls at a rate of 4.95% (ORs: 3.89 and 4.16).
Double heterozygotes had a clinical presentation intermediate between FVL and prothrombin (show F2 ELISA Kits) mutation single carriers.
increased frequency of factor V Leiden G1691A and prothrombin (show F2 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits)-mediated inactivation, and slightly reduced APC (show APC ELISA Kits) cofactor activity
Data suggest factor Xa (FXa (show F10 ELISA Kits)) and factor Va (FVa) compete to bind FXa (show F10 ELISA Kits) on both PS model membranes and microparticles from activated platelets; this competition between dimerization/prothrombinase (show FGL2 ELISA Kits) 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