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.
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.
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.
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.
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.
TL;DR: It is concluded that intact plasma will quickly replace the fibrinogen it has deposited on glass-like surfaces by high molecular weight kininogen and, to a smaller extent, by factor XII.