Suzuki K, Nishioka J, Matsuda M, Murayama H, Hashimoto S
J Biochem. 1984 Aug;96(2):455-60. doi: 10.1093/oxfordjournals.jbchem.a134857.
The prothrombin-converting activity of Factor Xa was enhanced by thrombin-stimulated Factor V-deficient platelets and supplementary extraneous Factor Va, and also by thrombin-stimulated normal human platelets. Both extraneous Factor Va and intra-platelet Factor Va were equally inactivated by a gamma-carboxyglutamic acid-containing plasma protease, activated protein C. However, a relatively larger amount of activated protein C was required for efficient inactivation of platelet-associated Factor Va as compared with the amount of activated protein C needed for inactivation of phospholipid vesicle-associated Factor Va. Protein S, another gamma-carboxyglutamic acid-containing plasma protein, increased the rate of the inactivation of platelet-associated Factor Va about 25-fold. This stimulating effect was observed only slightly with the thrombin-modified protein S. Thus, it was concluded that protein S is essential for the process of inactivation of platelet-associated Factor Va by activated protein C.
凝血酶刺激的缺乏因子V的血小板和补充的外源因子Va，以及凝血酶刺激的正常人血小板均可增强因子Xa的凝血酶原转化活性。外源因子Va和血小板内因子Va均可被含γ-羧基谷氨酸的血浆蛋白酶——活化蛋白C同等程度地灭活。然而，与灭活磷脂囊泡相关因子Va所需的活化蛋白C量相比，高效灭活血小板相关因子Va需要相对更多量的活化蛋白C。蛋白S是另一种含γ-羧基谷氨酸的血浆蛋白，可使血小板相关因子Va的灭活速率提高约25倍。仅在凝血酶修饰的蛋白S中观察到轻微的这种刺激作用。因此，得出结论，蛋白S对于活化蛋白C灭活血小板相关因子Va的过程至关重要。
