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f5

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Official Full Name
coagulation factor V (proaccelerin, labile factor)
Background
Factor V (pronounced factor five) is a protein of the coagulation system, rarely referred to as proaccelerin or labile factor. In contrast to most other coagulation factors, it is not enzymatically active but functions as a cofactor. Deficiency leads to predisposition for hemorrhage, while some mutations (most notably factor V Leiden) predispose for thrombosis. Coagulation factor V is a cofactor that participates with factor Xa to activate prothrombin to thrombin. Factor Va is composed of a heavy chain and a light chain, noncovalently bound. The interaction between the two chains is calcium-dependent. Thrombin activates factor V proteolytically to the active cofactor, factor Va (formation of a heavy chain at the N-terminus and a light chain at the C-terminus). Sulfation is required for efficient thrombin cleavage and activation and for full procoagulant activity. Defects in F5 are the cause of Owren parahemophilia which is an hemorrhagic diastesis. Defects in F5 are the cause of resistance to activated protein C (APCR). APCR is a form of thrombophilia. The APCR mutation is found in about 5% of the population which suggest that a slight thrombotic tendency may confer some advantage in fetal implantation.
Synonyms
F5; FVL; PCCF; coagulation factor V; factor V Leiden; OTTHUMP00000032547; OTTHUMP00000032548; proaccelerin, labile factor; activated protein c cofactor; coagulation factor V jinjiang A2 domain; coagulation factor V (proaccelerin, labile factor); wu:fd21h06; si:bz20i5.3; factor V

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:

  1. 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.
  2. 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.