|Gene Name||Approved Name||Aliases||Chromosome|
|C3AR1||complement C3a receptor 1||AZ3B, C3AR, HNFAG09||12p13.31|
|C5AR1||complement C5a receptor 1||C5A, C5AR, C5R1, CD88||19q13.32|
|C5AR2||complement component 5a receptor 2||C5L2, GPF77, GPR77||19q13.32|
The activation of the complement cascade produces a number of small fragments that are bioactive: potent chemoattractants and secretagogues that act on immune and non-immune cells. Similar peptides can also be released by the actions of non-complement proteases, for instance during clotting. Initially these were termed anaphylatoxins because of their effect on mast cell histamine release, but were reclassified as complement component peptides. They include C3a and C5a, which are involved immune response, neural development and organ regeneration. A third peptide, C4a, has a similar structure, but it is inactive in humans. Since the primary function of complement component peptides is in inflammation, they are important targets for the development of anti-inflammatory therapies.
The anaphylatoxin chemotactic receptors (also known as complement peptide receptors) are a group of rhodopsin-like G-protein coupled receptors (GPCRs). There are three subtypes: C3a receptor (C3AR1), C5a receptor (C5AR1) and C5a anaphylatoxin receptor C5L2 (C5AR2). Both C3AR1 and C5AR1 receptors are classical GPCRs. However, C5AR2 appears to be permanently uncoupled from G proteins but can associate with beta-arrestin. Nevertheless, it has been shown that activation of both C5AR1 and C5AR2 is required for a full pro-inflammatory response, particularly in mice. Several receptor antagonists have been reported, although none, so far, have been show to be effective in humans.
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