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Coagulation factor V

factor V Leiden, coagulation factor V, FVL
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. [provided by RefSeq, Oct 2008] (from NCBI)
Top mentioned proteins: HAD, AGE, methylenetetrahydrofolate reductase, CAN, OUT
Papers on factor V Leiden
Cryptogenetic liver cirrhosis and prothrombotic mutations - A mere association?
González Reimers et al., Spain. In Rev Esp Enferm Dig, Feb 2016
The coincidence in a given patient of prothrombotic mutations, such as factor V Leiden or PAI-1 polymorphisms, can accelerate the fibrogenetic process.
A risk score for prediction of recurrence in patients with unprovoked venous thromboembolism (DAMOVES).
Ruiz Giardín et al., Madrid, Spain. In Eur J Intern Med, Feb 2016
P=0.028) and heterozygous of factor V Leiden and/or Prothrombin G20210A mutation (HR=13.86
Uncertain thrombophilia markers.
Mannucci et al., Milano, Italy. In Thromb Haemost, Jan 2016
The main inherited thrombophilias include the plasma deficiencies of the natural anticoagulants antithrombin, protein C and S; the gain-of-function mutations factor V Leiden and prothrombin G20210A; some dysfibrinogenaemias and high plasma levels of coagulation factor VIII.
Interaction of Hereditary Thrombophilia and Traditional Cardiovascular Risk Factors on the Risk of Arterial Thromboembolism: Pooled Analysis of Four Family Cohort Studies.
Meijer et al., Groningen, Netherlands. In Circ Cardiovasc Genet, Jan 2016
Five hereditary thrombophilic defects including factor V Leiden, prothrombin G20210A defect and deficiencies of the natural anticoagulants (i.e., antithrombin, protein C and protein S) were assessed, and data on risk factors and previous ATE were collected.
Molecular characterization of novel splice site mutation causing protein C deficiency.
Imtiaz et al., Riyadh, Saudi Arabia. In Blood Coagul Fibrinolysis, Jan 2016
Analysis of factor V Leiden (G1691A) and factor II (G20210A) mutations was also done.
Left ventricular intracardiac thrombus in a patient with Behçet disease successfully treated with immunosuppressive agents without anticoagulation: a case report and review of the literature.
Nasonov et al., Moscow, Russia. In Rheumatol Int, Nov 2015
Known thrombophilic factors such as methylenetetrahydrofolate reductase gene mutations, factor V Leiden mutation, proteins S and C, antithrombin III, activated protein C resistance, and antiphospholipid antibodies may contribute to the formation of intracardiac thrombi in BD.
Management and outcome of pregnancies in women with antithrombin deficiency: a single-center experience and review of literature.
Boda et al., Debrecen, Hungary. In Blood Coagul Fibrinolysis, Oct 2015
Two women had additional factor V Leiden heterozygous mutations.
Endothelial Dysfunction and Altered Coagulation As Mediators of Thromboembolism in Behçet Disease.
Jiménez-Yuste et al., Madrid, Spain. In Semin Thromb Hemost, Sep 2015
These factors, together with the increased levels of homocysteine observed in BD patients, induce the endothelial cell expression of adhesion molecules (VCAM-1 and ICAM-1) and tissue factor; the release of cytokines, soluble CD40L (sCD40L), matrix metalloproteinase-9, and blood coagulation factor V; the inhibition of fibrinolysis; the disruption of nitric oxide metabolism; and the increase in platelet reactivity and lipid peroxidation.
Thrombophilia and venous thromboembolism in pregnancy: a meta-analysis of genetic risk.
Zintzaras et al., Providence, United States. In Eur J Obstet Gynecol Reprod Biol, Aug 2015
Three common polymorphic variants, namely Factor V Leiden (FVL), Prothrombin G20210A (PT G20210A) and Methylenetetrahydrofolate Reductase (MTHFR) C677T are candidate genes for venous thromboembolism (VTE) in pregnancy.
Activated protein C resistance assay and factor V Leiden.
Mangge et al., Graz, Austria. In N Engl J Med, 2014
The authors suggest that functional testing for activated protein C resistance is cheaper and more clinically relevant than genetic testing to detect a factor V Leiden mutation in identifying persons who are at risk for thromboembolism.
A bipartite autoinhibitory region within the B-domain suppresses function in factor V.
Camire et al., Philadelphia, United States. In J Biol Chem, 2012
an unexpected sequence-specific role for the B-domain of factor V negatively regulates function, preventing activity of the procofactor
Prevalence of 1691G>A FV mutation in Poland compared with that in other Central, Eastern and South-Eastern European countries.
Ciechanowicz et al., Szczecin, Poland. In Bosn J Basic Med Sci, 2012
the 1691G>A FV allele frequency in Poland, as well as other countries compared, is significantly lower than that in Czech
Role of factor V Leiden or G20210A prothrombin mutation in patients with symptomatic pulmonary embolism and deep vein thrombosis: a meta-analysis of the literature.
Prisco et al., In J Thromb Haemost, 2012
Letter/Meta-Analysis: suggest that FV Leiden patients are more likely to present with deep vein thrombosis than with isolated pulmonary embolism.
[Neonatal renal vein thrombosis in a heterozygous carrier of both factor V Leiden and the MTHFR gene mutation].
Sfar et al., Tunisia. In Arch Pediatr, 2012
We report a case of RVT in a newborn who was a heterozygous carrier of both factor V Leiden and the methylene tetrahydrofolate reductase (MTHFR) gene mutation.
[Additional mass on the intracardiac lead - diagnostic doubts and the optimal choice of treatment].
Lipiec et al., Łódź, Poland. In Kardiol Pol, 2011
case of a 30 year-old female with implantable cardioverter-defibrillator. One and a half year later the patient suffered from endocarditis and underwent surgery. The factor V Leiden mutation was diagnosed
Clotting factor gene polymorphisms and colorectal cancer risk.
Brenner et al., Heidelberg, Germany. In J Clin Oncol, 2011
Our results support a role of clotting factor polymorphisms and thereby the coagulation system in the risk of colorectal cancer.
Predictive value of factor V Leiden and prothrombin G20210A in adults with venous thromboembolism and in family members of those with a mutation: a systematic review.
Bass et al., Baltimore, United States. In Jama, 2009
OBJECTIVES: To define rates of recurrent VTE among adults with VTE with a factor V Leiden (FVL) or prothrombin G20210A mutation compared with those without such mutations; to define rates of VTE among family members of adults with a FVL or prothrombin G20210A mutation according to presence or absence of a mutation; and to assess whether testing adults with VTE for FVL or prothrombin G20210A improves outcomes.
Effect of hypobaric hypoxia, simulating conditions during long-haul air travel, on coagulation, fibrinolysis, platelet function, and endothelial activation.
Greaves et al., Leicester, United Kingdom. In Jama, 2006
Participants were screened for factor V Leiden G1691A and prothrombin G20210A mutation and were excluded if they tested positive.
Activation of coagulation system during air travel: a crossover study.
Rosendaal et al., Amsterdam, Netherlands. In Lancet, 2006
To study the effect of risk factors for thrombosis, we included participants with the factor V Leiden mutation (n=11), those who took oral contraceptives (n=15), or both (n=15), as well as 30 individuals with no specific risk factors.
Genetic Polymorphism of Epoxide Hydrolase and GSTM1 in Lung Cancer Susceptibility of Korean Population.
Ahn et al., In Cancer Res Treat, 2003
PCR and RFLP (restriction fragments length polymorphism) with restriction enzyme (RsaI) and automatic sequencing were used for mEPHX genotyping (T-->C, Tyr113His) in exon 3 and (A-->G, His139Arg) in exon 4. Looking for homozygous deletions of GSTM1, multiplex PCR with primers for the GSTM1 gene and coagulation factor V gene (as positive control) were performed.
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