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 H and C4-binding protein, and the cell membrane proteins, complement receptor 1 (CR1), 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 Cob. All are members of the regulators of the complement activation (RCA) gene cluster on human chromosome 1q32, and share a common 60–70-amino-acid short consensus repeat (SCR), containing four invariant cysteines that form two intra-SCR disulfide bonds (1).
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