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F5 encodes an essential cofactor of the blood coagulation cascade. Zusätzlich bieten wir Ihnen Coagulation Factor V Kits (63) und Coagulation Factor V Proteine (23) und viele weitere Produktgruppen zu diesem Protein an.
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Platelet-derived FV contributes to the control of angiogenesis and is likely associated with thrombin (zeige F2 Antikörper) generation in hind limb ischemia model.
These findings reveal a novel biological function and mechanism of the protein C (zeige PROC Antikörper) pathway in which protein S and the aPC (zeige APC Antikörper)-cleaved form of fV are cofactors for anti-inflammatory cell signaling by aPC (zeige APC Antikörper) 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 (zeige GLA Antikörper) deficiency and FVL or other thrombosis-related gene defect in patients with genetic severe early-onset thrombosis.
Data suggest that tissue factor (zeige F3 Antikörper) and factor V induction by LPS (zeige TLR4 Antikörper) 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 (zeige GLA Antikörper) 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.
increased frequency of factor V Leiden G1691A and prothrombin (zeige F2 Antikörper) 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 (zeige MTHFR Antikörper) 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 (zeige PROC Antikörper)-mediated inactivation, and slightly reduced APC (zeige APC Antikörper) cofactor activity
prothrombotic mutations in factor V Leiden and prothrombin (zeige F2 Antikörper) 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 (zeige APC Antikörper) are in spatially and kinetically distinct compartments, and that it is possible to specifically inhibit the anticoagulant activity of APC (zeige APC Antikörper). Targeting APC (zeige APC Antikörper) 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
The goal of this study was to evaluate the impact of EHR point-of-care tools on medical record documentation of genetic testing care processes for the common HFE (zeige HFE Antikörper) mutations, a thrombophilia panel, and HLA-B27 (zeige MRAP Antikörper).
Data suggest factor Xa (FXa (zeige F10 Antikörper)) and factor Va (FVa) compete to bind FXa (zeige F10 Antikörper) on both PS model membranes and microparticles from activated platelets; this competition between dimerization/prothrombinase (zeige FGL2 Antikörper) 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