Prothrombin is activated on the surface of a phospholipid membrane that binds the amino end of prothrombin and factors Va and , Xenopus/Amphibian,a in Ca-dependent interactions. Factor , Xenopus/Amphibian,a removes the activation peptide and cleaves the remaining part into light and heavy chains. The activation process starts slowly because factor V itself has to be activated by the initial, small amounts of thrombin. Thrombin, which cleaves bonds after Arg and Lys, converts fibrinogen to fibrin and activates factors V, VII, VIII, , Xenopus/Amphibian,III, and, in comple, Xenopus/Amphibian, with thrombomodulin,Porcinerotein C. Thrombin functions in blood homeostasis, inflammation and wound healing. Defects in thrombin are the cause of factor II deficiency (FA2D), a very rare blood coagulation disorder characterized by mucocutaneous bleeding symptoms. Genetic variations in thrombin are linked to ischemic stroke and to thrombosis (THR), a multifactorial disorder of hemostasis characterized by abnormal platelet aggregation in response to various agents and recurrent thrombi formation.