C5AR2

Protein-coding gene in the species Homo sapiens From Wikipedia, the free encyclopedia

Complement component 5a receptor 2 is a protein of the complement system that in humans is encoded by the C5AR2 gene.[5][6] It is highly expressed in the blood and spleen,[7] predominantly by myeloid cells.[8][9]

AliasesC5AR2, C5L2, GPR77, complement component 5a receptor 2, complement C5a receptor 2, C5a2
End47,347,329 bp[1]
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C5AR2
Identifiers
AliasesC5AR2, C5L2, GPR77, complement component 5a receptor 2, complement C5a receptor 2, C5a2
External IDsOMIM: 609949; MGI: 2442013; HomoloGene: 49549; GeneCards: C5AR2; OMA:C5AR2 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001271749
NM_001271750
NM_018485

NM_001146005
NM_176912

RefSeq (protein)

NP_001258678
NP_001258679
NP_060955

NP_001139477
NP_795886

Location (UCSC)Chr 19: 47.33 – 47.35 MbChr 7: 15.97 – 15.98 Mb
PubMed search[3][4]
Wikidata
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Function

The anaphylatoxins C3a and C5a are fragments of C3 and C5 generated via proteolytic cleavage by C3 convertases and C5 convertases during the complement cascade. They are pro-inflammatory mediators which bind to the anaphylatoxin receptors, C3aR, C5aR1 and C5aR2. The anaphylatoxin receptors are a family of three proteins which beloing to the G protein-coupled receptor superfamily. C3aR and C5aR1 bind C3a and C5a, respectively, which mediate a broad range of effects in host defense, including chemoattraction, vasodilation and immune cell activation.[10] C5aR2 binds C5a, but lacks GPCR activity,[11] and its function is less well understood.

C5aR2 was initially thought be a decoy receptor, acting as a sink for C5a to negatively regulate C5aR1 function.[11] However, more recent research has uncovered independent roles for C5aR2, including modulation of the innate immune response in myeloid cells,[12][13] translocation of C5a to drive transendothelial migration of neutrophils,[14] β-arrestin recruitment and modulation of ERK signalling[15][16] and modulation of lipid metabolism in obesity through C3a-desArg binding.[17] C5aR2 has been implicated in a broad range of inflammatory and infectious diseases.[18][19]

References

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