Tenase complex

Activated on surface of activated platelets by tenase complex (Ca, factors Villa and IXa) and by factor Vila in presence of tissue factor and Ca. ... 

Platelet membrane phosphatidylserine is critical to the formation of the tenase complex since on its surface activated factor VIII (Villa) generates a high-afflnity binding site for activated factor IX (IXa) in the presence of calcium. Subsequently, this complex activates factor X (2, 13). Platelet membrane phosphatidylserine similarly anchors activated factor V (Va), favoring the calcium-dependent binding of activated factor X (Xa). The prothrombinase complex is generated on the surface of the anionic platelet membrane phosphatidylserine when factor Va binds prothrombin. The prothrombinase complex cleaves prothrombin to produce thrombin, which has a multifunctional role (14). 

Sheehan JP, Lan H-C. Phosphorothioate oligonucleotides inhibit the intrinsic tenase complex. Blood 1998 92(5) 1617-25. 

Factor VEIa is the co-factor of factor IXa together they form the tenase complex which activates factor X, and so the cycle continues. 

The tenase complex is formed by the activated forms of the blood coagulation factors VIE and IX. It forms on a phospholipid surface in the presence of calcium and is responsible for the activation of factor X. Tenase is a contraction of ten and the suffix -ase , used for enzymes... 

PrekaUikrein is converted to kaUrkrem and factor XII is activated to Xlla. Factor Xlla activates Xl-XIa, which activates factor IX, which together with its co-factor Villa forms the tenase complex, resniting in activation of factor X. The minor role that the contact activation pathway has in initiating clot formation can he Ulnstrated hy the fact that patients with severe deficiencies of factor Xn, kininogen and prekaUikrein do not exhibit a bleeding disorder. 

Following activation by the contact factor or TF pathways, the coagulation cascade is maintained in a prothrombotic state by the continued activation of factors VIII and IX to form the tenase complex, until it is down-regulated by the anticoagulant pathways (see Section 11.9). 

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