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• W2912681052 abstract "CI inhibitor (C1Inh) activities could be divided into two categories:1.Vascular permeability is controlled through inhibition of two proteases of the contact system involved in bradykinin (BK) generation, factor XIIa (kon = 3.7 × 104 M−1•s−1) and plasma kallikrein (kon = 1.7 × 104 M−1•s−1).2.Antiinflammatory function is supported via control of complement (C1r, C1s, with kon = 43 × 104 M−1•s−1, and MASP2 with kon = 0.16 × 104 M−1•s−1) and the plasma contact system proteases, in addition to a competition mechanism involving its sialyl Lewisx and cell selectins, compromising interactions between inflammatory cells and endothelium. This is also consistent with the binding of C1Inh to endothelial cells.C1Inh also partially controls the intrinsic coagulation protease factor XI and thrombin, and the fibrinolytic proteases plasmin and tissue plasminogen activator, where C1Inh does not appear to play a significant role. Control of C1s is enhanced 30- to 60-fold by heparin, but heparin has no effect on the inhibition of factor XIIa or kallikrein. Basal serum concentration is 210–345 mg/L.Primary site of synthesis (cell type): The hepatocyte is the primary source of C1Inh for circulating C1Inh protein. Hereditary angioedema (HAE; phenotype MIM No 106100) is a rare inherited disease, which is clinically characterised by recurrent acute swelling episodes resulting from increased vascular permeability. Disruption of the SERPING1 gene by gene trapping enabled the generation of homozygous deficient mice." @default.
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• W2912681052 date "2018-01-01" @default.
• W2912681052 modified "2023-09-26" @default.
• W2912681052 title "C1 Inhibitor" @default.
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• W2912681052 doi "https://doi.org/10.1016/b978-0-12-810420-0.00023-7" @default.
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