Topic
Factor XII
About: Factor XII is a research topic. Over the lifetime, 1403 publications have been published within this topic receiving 53527 citations. The topic is also known as: Hageman factor & HAF.
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TL;DR: It has been shown that contact activates Factor XII (Hageman factor) perhaps by unfolding its molecule, which leads successively to the activation of Factors XI (PTA) and IX (Christmas factor), and X (Stuart–Prower factor), the evidence suggesting that all these reactions are enzymatic.
Abstract: AFTER years of confusion, it seems that a relatively simple pattern is emerging from present theories of blood coagulation. Its recognition is assisted by the Roman numeral terminology of the International Committee on Blood Clotting Factors, which, by displacing a profusion of synonyms, allows the basis of factual agreement to be seen. Physiological clotting seems to be initiated by contact of the blood with the ‘foreign’ surfaces presented by many substances and tissues other than normal vascular endothelium. Ratnoff et al.1–3, Margolis4,5, and others6–8 have established that contact activates Factor XII (Hageman factor) perhaps by unfolding its molecule, which leads successively to the activation of Factors XI (PTA) and IX (Christmas factor). It has now been shown that this is followed by the activation of Factors VIII (Antihaemophilic factor), and X (Stuart–Prower factor)9, the evidence suggesting that all these reactions are enzymatic.
941 citations
TL;DR: It is concluded that factor VII is most likely a zymogen, just as are the other proenzymes of the blood clotting process, and the kinetic constants obtained for the various coagulation reactions determined in vitro provide some insights into how these pathways may function in vivo.
801 citations
TL;DR: The data identify polyP as a new class of mediator having fundamental roles in platelet-driven proinflammatory and procoagulant disorders, including Hermansky-Pudlak Syndrome patients, who lack platelet polyP.
737 citations
TL;DR: These unexpected findings change the long-standing concept that the FXII-induced intrinsic coagulation pathway is not important for clotting in vivo and identify FXII as a novel target for antithrombotic therapy.
Abstract: Blood coagulation is thought to be initiated by plasma protease factor VIIa in complex with the membrane protein tissue factor. In contrast, coagulation factor XII (FXII)–mediated fibrin formation is not believed to play an important role for coagulation in vivo. We used FXII-deficient mice to study the contributions of FXII to thrombus formation in vivo. Intravital fluorescence microscopy and blood flow measurements in three distinct arterial beds revealed a severe defect in the formation and stabilization of platelet-rich occlusive thrombi. Although FXII-deficient mice do not experience spontaneous or excessive injury-related bleeding, they are protected against collagen- and epinephrine-induced thromboembolism. Infusion of human FXII into FXII-null mice restored injury-induced thrombus formation. These unexpected findings change the long-standing concept that the FXII-induced intrinsic coagulation pathway is not important for clotting in vivo. The results establish FXII as essential for thrombus formation, and identify FXII as a novel target for antithrombotic therapy.
692 citations
TL;DR: Data show that histone-activated platelets possess a procoagulant phenotype that drives plasma thrombin generation and suggest that TLR2 and TLR4 mediate the activation process.
688 citations