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Factor V Leiden (rs6025 or F5 p.R506Q [1]) is a variant (mutated form) of human factor V (one of several substances that helps blood clot), which causes an increase ...
14067 Ensembl ENSG00000198734 ENSMUSG00000026579 UniProt P12259 O88783 RefSeq (mRNA) NM_000130 NM_007976 RefSeq (protein) NP_000121 NP_032002 Location (UCSC) Chr 1: 169.51 – 169.59 Mb Chr 1: 163.98 – 164.05 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Coagulation factor V (Factor V), also less commonly known as proaccelerin or labile factor, is a protein involved in ...
Other blood clotting pathway mutations that increase the risk of clots include factor V Leiden. Prothrombin G20210A was identified in the 1990s. [2] About 2% of Caucasians carry the variant, while it is less common in other populations. [1] It is estimated to have originated in Caucasians about 24,000 years ago. [3]
[5] [9] The initiation phase accounts for less than 5% of total thrombin generation, making aPTT-based tests poorly indicative of hypercoagulability in general. [ 10 ] [ 11 ] The aPTT-based assay is more sensitive to levels of prothrombin and factor VIII , whereas the ETP-based test is more sensitive to levels of tissue factor pathway inhibitor ...
The last category, alterations in the constitution of blood, [6] has numerous possible risk factors such as hyperviscosity, coagulation factor V Leiden mutation, coagulation factor II G2021A mutation, deficiency of antithrombin III, protein C or S deficiency, nephrotic syndrome, changes after severe trauma or burn, cancer, late pregnancy and ...
The cancer stem cell model asserts that within a population of tumour cells, there is only a small subset of cells that are tumourigenic (able to form tumours). These cells are termed cancer stem cells (CSCs), and are marked by the ability to both self-renew and differentiate into non-tumourigenic progeny. The CSC model posits that the ...
Thromboembolism is a well-described complication of IBD, with a clinical incidence of up to 6% and a three-fold higher risk of disease, [31] [32] and the Factor V Leiden mutation further increases the risk of venous thrombosis. [33] Recent studies describe the co-occurrence between coeliac disease, in which IBD is common in venous thrombosis ...
The remaining copy of the tumor suppressor gene can be inactivated by a point mutation or via other mechanisms, resulting in a loss of heterozygosity event, and leaving no tumor suppressor gene to protect the body. Loss of heterozygosity does not imply a homozygous state (which would require the presence of two identical alleles in the cell).