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F5 encodes an essential cofactor of the blood coagulation cascade. Additionally we are shipping Coagulation Factor V Antibodies (113) and Coagulation Factor V Proteins (22) and many more products for this protein.
Showing 10 out of 51 products:
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
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 (show F3 ELISA Kits) and factor V induction by LPS (show TLR4 ELISA Kits) 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
Fetal gene defects precipitate platelet-mediated pregnancy failure in factor V Leiden mothers.
The FVL mutation has no effect on the development of secondary tumours of colon cancer in livers of mice.
Factor V (F5) c.1691G>A (Leiden) was present in 0.5% of 400 ischemic stroke patients in Sri (show SRI ELISA Kits) Lanka. F5 mutation was present in a statistically significant number of patients with venous thrombosis (P = .005) compared to those with arterial thrombosis.
The present data showed that FVL, MTHFR (show MTHFR ELISA Kits) polymorphisms also combined with thrombophilic gene mutations have a strong association with recurrent pregnancy loss.
FVL has a modifying effect on PAI-1 (show SERPINE1 ELISA Kits) polymorphism in relation to risk of VTE recurrence.
combination of FVL and MTHFR (show MTHFR ELISA Kits) mutation related to the risk of recurrent fetal death and habitual abortion
Case Report: acquired FV inhibitor that developed in a patient after exposure to human thrombin (show F2 ELISA Kits) used as a hemostatic agent during an otorhinolaryngology surgical procedure.
In the current study Factor V Leiden, prothrombin (show F2 ELISA Kits) G20210A, and thrombospondin-1 (show THBS1 ELISA Kits) polymorphisms showed no association with severity of hepatic fibrosis.
Chromosomal abnormalities and abnormalities in the genes related to thrombophilia such as FVL, MTHFR (show MTHFR ELISA Kits) and PTm mutations may be considered as risk factors for RM [recurrent miscarriage]
Given the essential role of platelet-derived factor Va in clot formation, understanding the cellular and molecular mechanisms that regulate how platelets acquire this molecule will be important for the treatment of excessive bleeding or clotting
the diagnosis of an 'unaffected' foetus was offered. The child was subsequently followed up after delivery and was found to be normal for factor V levels with a normal genotype
Data (including data from case-control, genetic association studies) suggest that Factor V mutation Leiden is associated with significant genetic predisposition for venous thromboembolism (not thrombophilia) in pregnancy. [META-ANALYSIS, REVIEW]
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