GPR77

C5a anaphylatoxin chemotactic receptor C5a2 also known as C5L2, G protein-coupled receptor 77, is a protein that in humans is encoded by the C5AR2 gene.[5][6]

C5AR2
Identifiers
Aliases	C5AR2, C5L2, GPF77, GPR77, complement component 5a receptor 2
External IDs	OMIM: 609949 MGI: 2442013 HomoloGene: 49549 GeneCards: C5AR2
Gene location (Human) Chr. Chromosome 19 (human)[1] Band 19q13.32 Start 47,332,175 bp[1] End 47,347,329 bp[1]
Gene location (Mouse) Chr. Chromosome 7 (mouse)[2] Band 7|7 A2 Start 16,234,585 bp[2] End 16,244,154 bp[2]
RNA expression pattern More reference expression data
Gene ontology Molecular function • GO:0001948 protein binding • signal transducer activity • complement component C5a receptor activity • G-protein coupled receptor activity Cellular component • integral component of membrane • cell membrane • basal plasma membrane • apical part of cell • membrane • integral component of plasma membrane Biological process • negative regulation of neutrophil chemotaxis • chemotaxis • G-protein coupled receptor signaling pathway • negative regulation of tumor necrosis factor production • regulation of interleukin-8 secretion • signal transduction • positive regulation of ERK1 and ERK2 cascade • positive regulation of epithelial cell proliferation • negative regulation of interleukin-6 secretion • regulation of complement activation • inflammatory response • phospholipase C-activating G-protein coupled receptor signaling pathway • positive regulation of cytosolic calcium ion concentration • complement component C5a signaling pathway • complement receptor mediated signaling pathway Sources:Amigo / QuickGO
Orthologs
Species	Human	Mouse
Entrez	27202	319430
Ensembl	ENSG00000134830	ENSMUSG00000074361
UniProt	Q9P296	Q8BW93
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 Mb	Chr 7: 16.23 – 16.24 Mb
PubMed search	[3]	[4]
Wikidata
View/Edit Human View/Edit Mouse

Function

The anaphylatoxins C3a, C4a, and C5a are cationic fragments generated during the complement cascade that participate in host defense. In the case of inappropriate complement activation, anaphylatoxins may be involved in autoimmunity and sepsis. C5a2 is coexpressed with the C5a receptor, (C5a1, C5aR, C5R1, CD88), on polymorphonuclear neutrophils and may modulate C5a1 activity.[6][7]

References

1. GRCh38: Ensembl release 89: ENSG00000134830 - Ensembl, May 2017
2. GRCm38: Ensembl release 89: ENSMUSG00000074361 - Ensembl, May 2017
3. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
4. "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
5. Lee DK, George SR, Cheng R, Nguyen T, Liu Y, Brown M, Lynch KR, O'Dowd BF (Feb 2001). "Identification of four novel human G protein-coupled receptors expressed in the brain". Brain Res Mol Brain Res. 86 (1–2): 13–22. doi:10.1016/S0169-328X(00)00242-4. PMID 11165367.
6. "HGNC:4527". Retrieved 2019-08-30.
7. Gerard NP, Lu B, Liu P, Craig S, Fujiwara Y, Okinaga S, Gerard C (December 2005). "An anti-inflammatory function for the complement anaphylatoxin C5a-binding protein, C5L2". J. Biol. Chem. 280 (48): 39677–80. doi:10.1074/jbc.C500287200. PMID 16204243.

Further reading

• Klos A, Wende E, Wareham KJ, Monk PN (2013). "International Union of Pharmacology. LXXXVII. Complement peptide C5a, C4a, and C3a receptors". Pharmacol. Rev. 65 (1): 500–43. doi:10.1124/pr.111.005223. PMID 23383423.
• Ohno M, Hirata T, Enomoto M, et al. (2000). "A putative chemoattractant receptor, C5L2, is expressed in granulocyte and immature dendritic cells, but not in mature dendritic cells". Mol. Immunol. 37 (8): 407–12. doi:10.1016/S0161-5890(00)00067-5. PMID 11090875.
• Cain SA, Monk PN (2002). "The orphan receptor C5L2 has high affinity binding sites for complement fragments C5a and C5a des-Arg(74)". J. Biol. Chem. 277 (9): 7165–9. doi:10.1074/jbc.C100714200. PMID 11773063.
• Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932.
• Kalant D, Cain SA, Maslowska M, et al. (2003). "The chemoattractant receptor-like protein C5L2 binds the C3a des-Arg77/acylation-stimulating protein". J. Biol. Chem. 278 (13): 11123–9. doi:10.1074/jbc.M206169200. PMID 12540846.
• Otto M, Hawlisch H, Monk PN, et al. (2004). "C5a mutants are potent antagonists of the C5a receptor (CD88) and of C5L2: position 69 is the locus that determines agonism or antagonism". J. Biol. Chem. 279 (1): 142–51. doi:10.1074/jbc.M310078200. PMID 14570896.
• Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The Status, Quality, and Expansion of the NIH Full-Length cDNA Project: The Mammalian Gene Collection (MGC)". Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMC 528928. PMID 15489334.
• Huber-Lang M, Sarma JV, Rittirsch D, et al. (2005). "Changes in the novel orphan, C5a receptor (C5L2), during experimental sepsis and sepsis in humans". J. Immunol. 174 (2): 1104–10. doi:10.4049/jimmunol.174.2.1104. PMID 15634936.
• Kalant D, MacLaren R, Cui W, et al. (2005). "C5L2 is a functional receptor for acylation-stimulating protein". J. Biol. Chem. 280 (25): 23936–44. doi:10.1074/jbc.M406921200. PMID 15833747.
• Johswich K, Martin M, Thalmann J, et al. (2007). "Ligand specificity of the anaphylatoxin C5L2 receptor and its regulation on myeloid and epithelial cell lines". J. Biol. Chem. 281 (51): 39088–95. doi:10.1074/jbc.M609734200. PMID 17068344.
• Scola AM, Higginbottom A, Partridge LJ, et al. (2007). "THE ROLE OF THE N-TERMINAL DOMAIN OF THE COMPLEMENT FRAGMENT RECEPTOR, C5L2, IN LIGAND BINDING". J. Biol. Chem. 282 (6): 3664–71. doi:10.1074/jbc.M609178200. PMC 2873560. PMID 17158873.

External links

• "Complement Peptide Receptors: C5a2". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology.

This article incorporates text from the United States National Library of Medicine, which is in the public domain.