F5

Official Full Name

coagulation factor V

Organism

Homo sapiens

GeneID

2153

Background

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]

Synonyms

FVL; PCCF; THPH2; RPRGL1;

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Detailed Information

Functions of F5

Coagulation factor V (F5) is the regulator of coagulation and anticoagulation pathways. It circulates as a single single-chaining factor, activated by thrombin FXa or FVa. And then becomes an auxiliary factor in the activation of the FXa. In addition, studies have shown that the activity of blood coagulation factor V plays an important role in reducing liver decompensation or severe liver disease, therefore, it is considered to be a good index for judging the prognosis of patients with liver disease. F5 activity is also closely related to the formation of blood clots. For this reason, it can be used as a predictor of portal vein thrombosis.

F5 and VTE

Thromboembolism, including venous thromboembolism (VTE), is a disease that severely damages human health. It is characterized by high morbidity, high disability rate, high misdiagnosis and missed diagnosis rate, and low detection rate. The diagnosis of pre-thrombotic condition is particularly important for the prevention and treatment of thrombotic diseases. Hyperhomocysteinaemia (HHcy) and activated protein C resistance (APCR) can induce the pre-thrombotic state, which can lead to the formation of thrombus. The mutation of coagulation factor V gene is the main cause of APCR.

When any part of the three stages of the clotting process is obstructed, it can cause coagulopathy. F5 is an auxiliary factor in the process of coagulation. Studies have found that mutations in the thrombin V gene (also known as the factor V Lei-den mutation) allow F5a to maintain the activity of coagulation and enhance the resistance to anticoagulant effect of the anticoagulant system APC.

F5 and Severe Hepatitis

The liver is the main synthetic organ of coagulation factor. It was found that patients with severe hepatitis have a significant decrease in coagulation factor synthesis due to the massive necrosis of the liver. The degree of reduction was positively correlated with the severity of liver damage. The order of decrease in the activity of clotting factor is VII, II, X, V. Consequently, it is more meaningful to select the factor V as the most important index for the reduction in patients with severe hepatitis.

References:

Li xiagao,et al. Correlation between thrombosis and prethrombotic status, and blood coagulation factor V gene polymorphism, APCR and HHcy. Journal of Experimental Hematology, 2016, 24( 6) : 1850-1855.
B. Dahlbäck, et al. Novel insights into the regulation of coagulation by factor V isoforms, tissue factor pathway inhibitor α, and protein. Wiley journal, 2017, 1241-1250.

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