prothrombinase


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Related to prothrombinase: Stuart-Prower factor

prothrombinase

 [pro-throm´bin-ās]
2. the complex formed between activated factor x and calcium, phospholipid, and modified factor v; it can cleave and activate prothrombin to thrombin in the common pathway of coagulation. The term is sometimes used to refer specifically to the active enzyme center of the complex, which is activated factor x.

fac·tor X

in the clotting of blood, also known as: Stuart factor, Stuart-Prower factor, prothrombase, and prothrombinase. Its active form, factor Xa (EC 3.4.21.6), is formed from factor X by limited proteolysis and assists in the conversion of prothrombin to thrombin. A deficiency of factor X will lead to impaired blood coagulation.

prothrombinase

(prō-thrŏm′bə-nās′, -nāz′)
n.
An enzyme complex that catalyzes the hydrolysis of prothrombin to thrombin.

fac·tor X

(fak'tŏr)
A plasma coagulation factor that assists in the conversion of prothrombin to thrombin. Deficiency impairs blood coagulation.
Synonym(s): prothrombinase, Stuart factor, Stuart-Prower factor.

fac·tor X

(fak'tŏr)
A plasma coagulation factor that assists in the conversion of prothrombin to thrombin.
Synonym(s): prothrombinase, Stuart factor, Stuart-Prower factor.
References in periodicals archive ?
Bleeding in patients with FV inhibitors may be difficult to treat, since FV inhibitors interfere with the prothrombinase complex and are difficult to bypass with currently available coagulation factor concentrates.
Raised [Ca.sup.2+] levels lead to the exposure of PS on the platelet surface that serves as a site for the assembly of intrinsic and extrinsic tenase and prothrombinase complexes; thus it is critical for thrombin generation in PRP [34].
Comple ment proteins C5b-9 cause release of membrane vesicles from the platelet surface that are enriched in the membrane receptor for coagulation factor Va and express prothrombinase activity.
The processes of prothrombinase formation on the 20th day after the 15-day intramuscular peptide [OFXG.sub.3] were accelerated.
Activity of the tissue factor/factor VIIa complex decreases 55% and prothrombinase complex declines by 70% as pH declines from 7.4 to 7.030.10 Plasma clotting times prolong as pH is reduced as well.
Platelet prothrombinase activity and intracellular calcium responses in patients with storage pool deficiency, glycoprotein IIb-IIIa deficiency, or impaired platelet coagulant activity-a comparison with Schott syndrome.
The brain contains the highest concentration of tissue thromboplastin in the body.[12] Thromboplastin activates Factor VII which initiates the extrinsic pathway, and in turn activates the prothrombinase complex which converts prothrombin to thrombin and then forms fibrin.
Methods based on the activation of coagulation at the prothrombinase level are unaffected (Table 4) (28, 29).
Rather, with vessel damage, tissue factor is exposed and complexes with factor Vila to generate prothrombinase (consisting of calcium, phospholipid, and activated factors X and V), which activates prothrombin to thrombin, which then generates fibrin from fibrinogen.
(147) Furihata et al demonstrate that an increased risk of arteriothrombotic disease is associated with an increased number of platelet collagen receptors (integrin [[alpha].sub.2][[beta].sub.1]) and increased concentration of glycoprotein II (GPII) and platelet prothrombinase activity.
Because pGPVI is the key to both types of responses, platelet aggregation and phosphatidylserine expression, loss of pGPVI-mediated phosphatidylserine exposure may result in reduced prothrombinase activity (24).