Activated factor XII

Factor Xlla converts prekallikrein to kallikrein and kallikrein cleaves HK to generate bradykinin. There is also an important positive feedback in the system in which the kallikrein generated rapidly converts unactivated factor XII to activated factor XII, and the rate of this reaction is hundreds of times faster than the rate of autoactivation [11]. Therefore, much of the unactivated factor XII can be cleaved and activated by kallikrein. Cl inhibitor inhibits all functions of factor Xlla and it is one of two major plasma kallikrein inhibitors. Thus all functions of kallikrein are also inhibited, including the feedback activation of factor XII, the cleavage of HK, and the activation of plasma pro-urokinase [66] to lead to plasmin formation. Cl inhibitor also inhibits the fibrinolytic enzyme plasmin, although it is a relatively minor inhibitor compared to a2-antiplasmin or a2-macroglobulin. 

Becker, C. G., Van Hamont, N., Wagner, M., Tobacco, cocoa, coffee and ragweed Crossreacting allergens that activate factor-XII-dependent pathways, Blood, 58, 861, 1981. (CA96 33194b)... 

Activated factor XII leads to the activation of factor XI in turn, activated factor XI, along with Ca++ ions and factor IV, leads to activation of factor IX. Activated factor IX, along with Ca++ ions, factor VIII, and PF3, leads to the activation of factor X. From the point of factor X activation, the extrinsic and intrinsic mechanisms follow the same pathway to fibrin formation. 

The effects of Lp(a) on the fibrinolytic system are based on the homology between plasminogen and Lp(a) (E3, E5, K4). Inactive Glu-plasminogen is converted to inactive glutamine-plasmin or inactive lysine-plasmin. Both can be converted to active lysine-plasmin, the activity of which is based on the serine protease part that splits fibrin and fibrinogen, but also factors V and Villa. In addition, Lp(a) is able to activate factor XII, factor VII, and the complement factors Cl and C3. 

Bouma BN, Miles LA, Beretta G et al (1980) Fluman plasma prekallikrein. Studies of its activation by activated factor XII and of its inactivation by diisopropyl phosphofluoridate. Biochemistry 19 1151-1160... 

Able to break down fibrin clots, cleave complement protein C3 and activate factor XII. 

FactorX can also be activated by kallikrein - in turn prekallikrein is activated to kallikrein by activated Factor XII, thus prolonging the initial contact activation of Factor XII. 

Activation of factor XII leads to complex events (30) connecting several areas of physiology. Interfaces accidentally introduced are sometimes ignored. For example, the surface of bacteria may activate factor XII (31) and thus be responsible for the finding that immune complex activates factor XII directly. There is the lack of strict specificity in the actions of several enzymes. For example, factor XII is needed for the conversion of prekallikrein (perhaps identical with Fletcher factor) to kallikrein by glass (32). Then conversion of kininogen to kinin by kalli-krein follows but several precursors may activate themselves as well as others (33). 

The pain-producing factor formed by diluting plasma may be identical with activated factor XII (Xlla) and splits into prekallikrein activator with factor XII activity and some fragments (34). Collagen gains kinin-... 

Antibody/antigen complex itself may not adsorb and activate factor XII (31), but its formation leads to activation of complement factor Ce which in turn may activate clotting (40, 41). Here too, some products appear poorly soluble and may offer physical interfaces rather than chemical activity. 

In damaged tissue, the proteins kininogen and kallikrein activate factor XII (part of the intrinsic pathway). 

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