Coagulation Factor V (F5) ELISA Kits

F5 encodes an essential cofactor of the blood coagulation cascade. Zusätzlich bieten wir Ihnen Coagulation Factor V Antikörper (146) und Coagulation Factor V Proteine (24) und viele weitere Produktgruppen zu diesem Protein an.

list all ELISA KIts Gen GeneID UniProt
F5 14067 O88783
F5 2153 P12259
F5 304929  
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Katalog Nr. Reaktivität Sensitivität Bereich Bilder Menge Lieferzeit Preis Details
Maus 45 pg/mL 125 pg/mL - 8000 pg/mL 96 Tests 13 bis 16 Tage
Human 0.78 ng/mL 3.12-200 ng/mL Typical standard curve 96 Tests 13 bis 16 Tage
Schwein 0.027 0.027 Typical standard curve 96 Tests 15 bis 18 Tage
Ratte 0.058 ng/mL 0.15 ng/mL - 10 ng/mL 96 Tests 13 bis 16 Tage
Affe 1.0 pg/mL 50-1000 pg/mL 96 Tests 15 bis 18 Tage
Kaninchen 1.0 pg/mL 50-1000 pg/mL   96 Tests 15 bis 18 Tage
Meerschweinchen 0.1 ng/mL 0.5-10 ng/mL   96 Tests 15 bis 18 Tage
Hund 0.1 ng/mL 0.5-10 ng/mL   96 Tests 15 bis 18 Tage
  96 Tests 15 bis 18 Tage
  96 Tests 15 bis 18 Tage

Am meisten referenzierte Coagulation Factor V ELISA Kits

  1. Mouse (Murine) Coagulation Factor V ELISA Kit für Sandwich ELISA - ABIN415764 : Wang, Braun, Zhang, Norström, Thorlacius: Thrombin generation in abdominal sepsis is Rho-kinase-dependent. in Biochemical and biophysical research communications 2015 (PubMed)
    Show all 2 Pubmed References

  2. Mouse (Murine) Coagulation Factor V ELISA Kit für 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 (PubMed)

Weitere ELISA Kits für Coagulation Factor V Interaktionspartner

Mouse (Murine) Coagulation Factor V (F5) Interaktionspartner

  1. Mice with the FVL mutation do not have increased spermatogenesis as compared to wildtype mice.

  2. Platelet-derived FV is a critical mediator of arterial thrombosis that involves platelet activation.

  3. Platelet-derived FV contributes to the control of angiogenesis and is likely associated with thrombin generation in hind limb ischemia model.

  4. These findings reveal a novel biological function and mechanism of the protein C pathway in which protein S and the aPC-cleaved form of fV are cofactors for anti-inflammatory cell signaling by aPC in the context of endotoxemia and infection

  5. Mice deficient in LMAN1 exhibit FV and FVIII deficiencies and liver accumulation of alpha1-antitrypsin.

  6. The FVL mutation does not influence coagulation activation, lung inflammation or survival in lethal influenza A.

  7. It suggested that there could be a combination of GLA deficiency and FVL or other thrombosis-related gene defect in patients with genetic severe early-onset thrombosis.

  8. 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.

  9. that the murine platelet FV compartment is derived exclusively from primary biosynthesis within cells of marrow origin and an intact platelet FV pool is not required for protection from spontaneous hemorrhage or bleeding following minor trauma

  10. the murine platelet and plasma FV pools are biosynthetically distinct

  11. The source of the FVL leading to accelerated thrombosis appears to be circulating, non-platelet-derived plasma FVL.

  12. 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.

  13. observations demonstrate a synergistic interaction between alpha-galactosidase A deficiency and Factor V Leiden toward tissue fibrin deposition; concomitant mutations in these genes may increase the penetrance of vascular thrombotic events in humans

  14. Fetal gene defects precipitate platelet-mediated pregnancy failure in factor V Leiden mothers.

  15. The FVL mutation has no effect on the development of secondary tumours of colon cancer in livers of mice.

  16. FV Leiden allele has no effect in murine colitis and we thus question the importance of activated blood coagulation in the etiology or pathogenesis of inflammatory bowel disease.

  17. the factor V Leiden mutation is associated with enhanced thrombotic tendency after FeCl3 injury of the femoral artery on a standard fat diet, but not a high fat diet

  18. In contrast to humans, pregnancy induced a decrease in APC resistance in wild-type and in FV Leiden mice.

  19. Homozygous Factor V could promote atherosclerosis and fibrin deposition in apolipoprotein E deficient mice.

Human Coagulation Factor V (F5) Interaktionspartner

  1. High prevalence of Factor V Leiden 1691G/A variation in preeclamptic patients compared to controls suggest an involvement of this variation in predisposing to preeclampsia in this setting.

  2. association of Factor V Leiden with sickle cell disease not found in Tunisian patients

  3. The decreased rate of coagulation factor V rs9287090 allele A, rs1046712 allele T, and rs1800594 allele G may contribute to the susceptibility to unexplained recurrent spontaneous abortion among ethnic Han Chinese from Wenzhou area.

  4. The F5 G1691A polymorphism was associated with lacunar stroke. The F2 G20210A polymorphism was associated with stroke due to thrombosis of the brachiocephalic arteries

  5. Occlusion of anion-binding exosite 2 in meizothrombin explains its impaired ability to activate factor V.

  6. Heterozygosity for FVL is associated with Recurrent Venous Thromboses.

  7. In this document, we will focus on genetic testing for factor V Leiden and factor II c.*97G>A variants

  8. No significant difference in FVL genotype between patients and controls was observed, whereas high frequencies of PRT G20210A, MTHFR C677T and MTHFR A1298C mutations in the Hb S patients

  9. factor V Leiden and MTHFR C677T polymorphisms were significantly associated with recurrent pregnancy loss (RPL) in Bosnian women...

  10. 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 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.

  11. 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

  12. suggesting that the FVL paradox is related to the carriership of one wild type and one mutated factor V allele

  13. Review/Meta-analysis: Factor V G1691A single nucleotide gene polymorphism was associated with risk of ischemic stroke mainly in young adults.

  14. Factor V Leiden mutation is associated with venous thromboembolism in cancer.

  15. we were not able to confirm the association between the polymorphisms of f5, f2, and mthfr and pregnancy loss in Bosnian women

  16. 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).

  17. contribution of FVLeiden causing resistance to activated protein C in Indian population is not as strong as previously reported in Western countries

  18. 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.

  19. 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).

  20. Double heterozygotes had a clinical presentation intermediate between FVL and prothrombin mutation single carriers.

Cow (Bovine) Coagulation Factor V (F5) Interaktionspartner

  1. Data suggest factor Xa (FXa) and factor Va (FVa) compete to bind FXa on both PS model membranes and microparticles from activated platelets; this competition between dimerization/prothrombinase complex formation appears to regulate blood coagulation.

Coagulation Factor V (F5) Antigen-Profil

Beschreibung des Gens

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.

Genbezeichner und Symbole assoziert mit Coagulation Factor V (F5) ELISA Kits

  • coagulation factor V (f5) Antikörper
  • coagulation factor V (F5) Antikörper
  • Ac2-120 Antikörper
  • AI173222 Antikörper
  • Cf-5 Antikörper
  • Cf5 Antikörper
  • FVL Antikörper
  • PCCF Antikörper
  • RPRGL1 Antikörper
  • THPH2 Antikörper

Bezeichner auf Proteinebene für Coagulation Factor V (F5) ELISA Kits

coagulation factor V , activated protein C cofactor , activated protein c cofactor , coagulation factor V jinjiang A2 domain , factor V Leiden , proaccelerin, labile factor

100534566 Oreochromis niloticus
14067 Mus musculus
2153 Homo sapiens
304929 Rattus norvegicus
280687 Bos taurus
100715882 Cavia porcellus
397217 Sus scrofa
100685858 Canis lupus familiaris
101123649 Ovis aries
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