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- W1503881313 abstract "Factor XII (FXII) is a serine protease that was thought to initiate hemostasis. However, FXII-deficient patients do not have a bleeding state. Recent investigations have begun to define FXII's physiologic activities. FXII is a multidomain protein. Its light chain contains its proteolytic function that activates factor XI, prekallikrein, and the classic pathway of complement. FXII also has the unique ability to autoactivate to a serine protease (FXIIa) when exposed to neutral or negatively charged biologic or artificial surfaces. In vivo, FXII/FXIIa deficiency influences thrombosis risk and inflammation. FXII's heavy chain consists of collagen and fibronectin binding domains, two EGF domains, and a proline-rich region. The FXII gene is structurally most similar to hepatocyte growth factor. FXII's heavy chain binds to uPAR, gC1qR, and cytokeratin 1. Through uPAR and β1 integrins, FXII induces ERK1/2 and AktS473 phosphorylation, promoting cell growth and angiogenesis. In vivo, FXII-deleted mice have reduced angiogenesis and are protected from venous thrombosis and arterial thrombosis induced by contact activation. These combined recent studies suggest that FXII contributes to vascular well-being and vascular health." @default.
- W1503881313 created "2016-06-24" @default.
- W1503881313 creator A5028267096 @default.
- W1503881313 creator A5066630966 @default.
- W1503881313 date "2014-02-14" @default.
- W1503881313 modified "2023-09-26" @default.
- W1503881313 title "Factor XII Deficiency or Hageman Factor Deficiency" @default.
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- W1503881313 doi "https://doi.org/10.1002/9781118833391.ch9" @default.
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