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- W3142093837 abstract "The complement system is tightly controlled by a number of plasma and intrinsic membrane proteins. A focal point of regulation is at the level of C3/C5 convertases. This occurs through the actions of the plasma proteins, factor Hand C4-binding protein, and the cell membrane proteins, complementreceptor 1 (CRl), decay accelerating factor (DAF), and membrane cofactor protein (MCP). These proteins inhibit C3/C5 convertases by accelerating their intrinsic decay and/or by acting as a factor I cofactor for the cleavage and inactivation of C3b and C4b. All are members of the regulators of the complement activation (RCA) gene cluster on human chromosome 1 q32, and share a common 60-70-amino-acid short consensus repeat (SCR), containing four invariant cysteines that form two intra-SCR disulfide bonds (1). As has been presented in previous chapters and will again be emphasized here, despite the ubiquitous presence of complement regulators, complement activation can occur in a diversity of pathological conditions. Evidently, in these states, the tempo of comple-" @default.
- W3142093837 created "2021-04-13" @default.
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- W3142093837 date "2012-01-01" @default.
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- W3142093837 title "Modulation of Disease Using Recombinant Human Endogenous Complement Inhibitors" @default.
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