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Blood factor XII

Griffin JH Role of surface in surface-dependent SO activation of Hageman factor (blood coagulation factor XII). Proc Natl Acad Sci USA 1978 75 1998-2002. [Pg.81]

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)... [Pg.162]

The fluidity of blood is a result of the inhibition of a complex series of enzymic reactions in the coagulation cascade (see Fig. 10). When triggered either intrinsically (by contact with foreign surfaces ), or extrinsically (by tissue factors from damaged cells), inactive proenzymes (factors XII, XI, IX, and X) are transformed into activated pro-teinases (XHa, XIa, IXa, and Xa, respectively). Each proteinase catalyzes the activation of the following proenzyme in the sequence, up to formation of thrombin (Factor Ha), another proteinase that catalyzes partial... [Pg.117]

Figure 17.1 Summary of the four cascades that result from trauma or bleeding and the reactions they catalyse. These are all activated by the blood clotting factor, Xlla (also known as the Hageman factor). Details of each cascade are presented in Figures 17.2, 17.4 and 17.6. Factor XII is activated by collagen and negatively charged surfaces to form the active form, Xlla. Figure 17.1 Summary of the four cascades that result from trauma or bleeding and the reactions they catalyse. These are all activated by the blood clotting factor, Xlla (also known as the Hageman factor). Details of each cascade are presented in Figures 17.2, 17.4 and 17.6. Factor XII is activated by collagen and negatively charged surfaces to form the active form, Xlla.
Intrinsic pathway All the protein factors necessary for coagulation are present in circulating blood. Clot formation may take several minutes and is initiated by activation of factor XII. [Pg.111]

Ellagic acid [476-66-4] - [COSMETICS] (Vol 7) -Factor XII activators [BLOOD, COAGULANTS AND ANTICOAGULANTS] (Vol 4)... [Pg.359]

FRACTIONATION,BLOOD - PLASMA FRACTIONATION] (Vol 11) Factor XII [9001-30-3], (See also Hageman factor.)... [Pg.390]

Heparin [9005-49-6] - [CARBOHYDRATES] (Vol 4) -Factor XII activators pLOOD, COAGULANTS AND ANTICOAGULANTS] (Vol 4) -sulfurm [MINERALNUTRIENTS] (Vol 16) -use m blood fractionation pRACTIONATION, BLOOD - PLASMA FRACTIONATION] (Vol 11) -use with cardiovascular agents [CARDIOVASCULARAGENTS] (Vol 5) -use with enzymes pNZYTffi APPLICATIONS - THERAPEUTIC] (Vol 9) -in white blood cells [AUTOMATED INSTRUMENTATION - HEMATOLOGY] (Vol 3)... [Pg.469]

The blood coagulation cascade. Each of the curved red arrows represents a proteolytic reaction, in which a protein is cleaved at one or more specific sites. With the exception of fibrinogen, the substrate in each reaction is an inactive zymogen except for fibrin, each product is an active protease that proceeds to cleave another member in the series. Many of the steps also depend on interactions of the proteins with Ca2+ ions and phospholipids. The cascade starts when factor XII and prekallikrein come into contact with materials that are released or exposed in injured tissue. (The exact nature of these materials is still not fully clear.) When thrombin cleaves fibrinogen at several points, the trimmed protein (fibrin) polymerizes to form a clot. [Pg.177]

Naito K, Fujikawa K, Activation of human blood coagulation factor XI independent of factor XII factor XI is activated by thrombin and factor Xia in the presence of negatively charged surfaces. J Biol Chem 1991 66 7353-7358. [Pg.23]

Figure 6. Triggering of kinin formation, blood coagulation, and fibrinolysis through specific proteolytic activation of the Hageman Factor (Factor XII). In the cascades, the factor on the left side of the reaction (zymogen) is converted to an active enzyme by proteolysis. PL = phospholipids. Figure 6. Triggering of kinin formation, blood coagulation, and fibrinolysis through specific proteolytic activation of the Hageman Factor (Factor XII). In the cascades, the factor on the left side of the reaction (zymogen) is converted to an active enzyme by proteolysis. PL = phospholipids.
Figure 5.3. Intrinsic and extrinsic blood clotting cascades. Factor I, fibrinogen Factor II, prothrombin (vitamin K-dependent) Factor III, thromboplastin Factor V, proac-celerin Factor VII, proconvertin (vitamin K-dependent) Factor VIII, antihemophilic factor Factor IX, Christmas factor (vitamin K-dependent) Factor X, Stnart factor (vitamin K-dependent) Factor XI, plasma thromboplastin Factor XII, Hageman factor Factor XIII, fibrin-stabilizing factor and Factor XIV, protein C (vitamin K-dependent). What was at one time called Factor IV is calcinm no factor has been assigned nnmber VI. Figure 5.3. Intrinsic and extrinsic blood clotting cascades. Factor I, fibrinogen Factor II, prothrombin (vitamin K-dependent) Factor III, thromboplastin Factor V, proac-celerin Factor VII, proconvertin (vitamin K-dependent) Factor VIII, antihemophilic factor Factor IX, Christmas factor (vitamin K-dependent) Factor X, Stnart factor (vitamin K-dependent) Factor XI, plasma thromboplastin Factor XII, Hageman factor Factor XIII, fibrin-stabilizing factor and Factor XIV, protein C (vitamin K-dependent). What was at one time called Factor IV is calcinm no factor has been assigned nnmber VI.
Figure 10.37. Blood-Clotting Cascade. A fibrin clot is formed by the interplay of the intrinsic, extrinsic, and final common pathways. The intrinsic pathway begins with the activation of factor XII (Hageman factor) by contact with abnormal surfaces produced by injury. The extrinsic pathway is triggered by trauma, which activates factor VII and releases a lipoprotein, called tissue factor, from blood vessels. Inactive forms of clotting factors are shown in red their activated counterparts (indicated by the subscript "a") are in yellow. Stimulatory proteins that are not themselves enzymes are shovm in blue. A striking feature of this process is that the activated form of one clotting factor catalyzes the activation of the next factor. Figure 10.37. Blood-Clotting Cascade. A fibrin clot is formed by the interplay of the intrinsic, extrinsic, and final common pathways. The intrinsic pathway begins with the activation of factor XII (Hageman factor) by contact with abnormal surfaces produced by injury. The extrinsic pathway is triggered by trauma, which activates factor VII and releases a lipoprotein, called tissue factor, from blood vessels. Inactive forms of clotting factors are shown in red their activated counterparts (indicated by the subscript "a") are in yellow. Stimulatory proteins that are not themselves enzymes are shovm in blue. A striking feature of this process is that the activated form of one clotting factor catalyzes the activation of the next factor.

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See also in sourсe #XX -- [ Pg.330 , Pg.331 , Pg.332 ]




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Factor XII

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