beta-Sitosterol, Antitumor agent

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

Prothrombin also known as coagulation factor II is an important protein in blood clotting with an approximate mass of 72 kDa. This protein is synthesized in the liver and is expressed mainly in the plasma as an inactive precursor of thrombin. Prothrombin plays a pivotal role in the conversion into active thrombin through factor X activation in the presence of ionized calcium and phospholipid surfaces. Thrombin then further acts to convert fibrinogen into fibrin leading to clot formation. Prothrombin also can interact with various cellular receptors influencing other pathways beyond coagulation.

Biological function summary

Prothrombin regulates hemostasis and is part of the prothrombinase complex along with factor Xa factor Va calcium ions and phospholipids. This complex allows for the precise regulation of thrombin generation on the surface of activated platelets. By controlling the formation of thrombin prothrombin affects not only blood coagulation but also influences cell proliferation inflammation and tissue repair. The careful balance of prothrombin activation is important to prevent excessive bleeding or clot formation.

Pathways

Prothrombin is an essential component of the coagulation cascade especially the intrinsic and extrinsic coagulation pathways. In these pathways it links with proteins such as fibrinogen and factor X contributing to the amplification and perpetuation of thrombin generation. Additionally thrombin produced from prothrombin engages in a feedback loop to further enhance factor V VIII and XI activation. Through these actions prothrombin helps maintain normal coagulation but must be tightly regulated to prevent thrombotic complications.

Associated diseases and disorders

Prothrombin is implicated in conditions like prothrombin thrombophilia and liver disease. Prothrombin thrombophilia is a genetic disorder that increases the risk for venous thromboembolism due to the presence of the G20210A mutation in the prothrombin gene. Moreover impaired prothrombin synthesis can occur as a result of liver disease leading to a higher bleeding risk. In thrombotic conditions proteins like protein C and antithrombin work to combat excessive prothrombin-generated thrombin underlining the necessity for balance and regulation in hemostatic processes.