C3a (complement)

C3a is one of the proteins formed by the cleavage of complement component 3; the other is C3b. C3a is a 77 residue anaphylatoxin that binds to the C3a receptor (C3aR), a class A G protein-coupled receptor. It plays a large role in the immune response.

C3a molecules induce responses through the GPCR C3a receptor. Like other anaphylatoxins, C3a is regulated by cleavage of its carboxy-terminal arginine, which results in a molecule with lowered inflammatory function (C3a desarginine).

C3a is an effector of the complement system with a range of functions including T cell activation and survival,angiogenesis stimulation,chemotaxis, mast cell degranulation, and macrophage activation. It has been shown to have both proinflammatory and anti-inflammatory responses, its activity able to counteract the proinflammatory effects of C5a.

C3a is a strongly basic and highly cationic 77 residue protein with a molecular mass of approximately 10 kDa. Residues 17-66 are made up of three anti-parallel helices and three disulfide bonds, which confer stability to the protein. The N-terminus consists of a fourth flexible helical structure, while the C terminus is disordered. C3a has a regulatory process and a structure homologous to complement component C5a, with which it shares 36% of its sequence identity.

C3a induces an immunological response through a 482 residue G-protein-coupled receptor called C3aR. The C3aR is similarly structurally homologous to C5aR, but contains an extracellular domain with more than 160 amino acids. Specific binding sites for interactions between C3a and C3aR are unknown, but it has been shown that sulfation of tyrosine 174, one of the amino acids in the extracellular domain, is required for C3a binding. It has also been demonstrated that the C3aR N terminus is not required for ligand binding.

C3a formation occurs through activation and cleavage of complement component 3 in a reaction catalyzed by C3-convertase. There are three pathways of activation, each of which leads to the formation of C3a and C3b, which is involved in antigen opsonization. Other than the alternative pathway, which is constantly active, C3a formation is triggered by pathogenic infection.

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