CD55 (DAF) binds C3bBb, C4bC2a

Stable Identifier
Reaction [transition]
Homo sapiens
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Decay-accelerating-factor (DAF, CD55) is a membrane- bound complement regulatory protein that inhibits autologous complement cascade activation. It is expressed on all cells that are in close contact with serum complement proteins, but also on cells outside the vascular space and on tumour cells. DAF binds to C3bBb and C4bC2a on cell surfaces, accelerating their dissociation and thereby inhibiting the amplification of complement. DAF can bind C3b and Bb, and must bind both for efficient decay acceleration. Although it can bind the inactive proenzymes C3b and C4b, the regulatory function of DAF is believed to be inhibition of activated C3 convertase enzymes (Harris et al. 2007).
Literature References
PubMed ID Title Journal Year
17182573 Decay-accelerating factor must bind both components of the complement alternative pathway C3 convertase to mediate efficient decay

Lea, SM, Pettigrew, DM, Morgan, BP, Harris, CL

J Immunol 2007
11694537 Decay-accelerating factor (DAF), complement receptor 1 (CR1), and factor H dissociate the complement AP C3 convertase (C3bBb) via sites on the type A domain of Bb

Atkinson, JP, Kuttner-Kondo, LA, Medof, ME, Mitchell, L, Hourcade, DE

J Biol Chem 2002
2420889 Endogenous association of decay-accelerating factor (DAF) with C4b and C3b on cell membranes

Kinoshita, T, Medof, ME, Nussenzweig, V

J Immunol 1986
Orthologous Events
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