Vitamin K-dependent zymogen

Protein C A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and Villa at the rate-limiting steps of thrombin formation. [NIH]... 

Protein G. This vitamin K-dependent glycoproteia serine protease zymogen is produced ia the Hver. It is an anticoagulant with species specificity (19—21). Proteia C is activated to Proteia by thrombomodulin, a proteia that resides on the surface of endothefial cells, plus thrombin ia the presence of calcium. In its active form, Proteia selectively iaactivates, by proteolytic degradation. Factors V, Va, VIII, and Villa. In this reaction the efficiency of Proteia is enhanced by complex formation with free Proteia S. la additioa, Proteia activates tissue plasminogen activator, which... 

Factor XIa in the presence of activates factor IX (55 kDa, a zymogen containing vitamin K-dependent y-carboxyglutamate [Gla] residues see Chapter 45), to the serine protease, factor IXa. This in turn cleaves an Arg-Ile bond in factor X (56 kDa) to produce the two-chain serine protease, factor Xa. This latter reaction requires the assembly of components, called the tenase... 

Protein C, another vitamin K-dependent serine protease zymogen in plasma, is a regulatory protein that, when activated, limits the activity of two activated procoagulant co-factors, factors Va and Villa. Heterozygotes for hereditary isolated protein C deficiency tend to develop a thrombotic disease which has been successfully treated with long-term coumarins (2,3). Apparently, the... 

Protein C, like Factors II, VII, IX, and X, is a vitamin K-dependent protein. Activated protein C (PCa) can be derived by limited proteolysis of this zymogen by thrombin, trypsin, or by Russell s viper venom (VI). PCa, in contrast to the other vitamin K—activated ctors, exerts an anticoagulant activity by inhibiting Factors Va and Villa (Fll). A second activity identified for PCa is the release of plasminogen activator based on animal in vivo studies (CIO, Z2). These biochemical observations and the discovery of patients vnth recurrent thrombosis who are congenitally deficient in protein C make PCa a candidate for a central role in hemostasis (BIT). 

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