C5a receptor

C5AR1
Identifiers
AliasesC5AR1, C5A, C5AR, C5R1, CD88, complement component 5a receptor 1, C5a receptor, complement C5a receptor 1
External IDsOMIM: 113995; MGI: 88232; HomoloGene: 20413; GeneCards: C5AR1; OMA:C5AR1 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001736

NM_001173550
NM_007577

RefSeq (protein)

NP_001727

NP_001167021
NP_031603

Location (UCSC)Chr 19: 47.29 – 47.32 MbChr 7: 15.98 – 15.99 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

The C5a receptor also known as complement component 5a receptor 1 (C5AR1) or CD88 (Cluster of Differentiation 88) is a G protein-coupled receptor for C5a. It functions as a complement receptor.[5] C5a receptor 1 modulates inflammatory responses, obesity, development and cancers.[6][7][8] From a signaling transduction perspective, C5a receptor 1 activation is implicated in β-arrestin2 recruitment via Rab5a,[9] coupling of Gαi proteins,[10] ERK1/2 phosphorylation, [11] calcium mobilization and Rho activation[12] leading to downstream functions, such as secretion of cytokines, chemotaxis, and phagocytosis.

C5a receptor structure and its residues possessing role in ligand binding or signaling.

Cells

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The C5a receptor 1 is expressed on:[13]

Agonist and antagonists

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Potent and selective agonist and antagonists for C5a receptor 1 have been developed.[14][15][16][17][18][19]

See also

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References

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  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000197405Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000049130Ensembl, 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. ^ Gerard C, Gerard NP (1994). "C5A anaphylatoxin and its seven transmembrane-segment receptor". Annual Review of Immunology. 12: 775–808. doi:10.1146/annurev.iy.12.040194.004015. PMID 8011297.
  6. ^ Brennan FH, Gordon R, Lao HW, Biggins PJ, Taylor SM, Franklin RJ, et al. (April 2015). "The Complement Receptor C5aR Controls Acute Inflammation and Astrogliosis following Spinal Cord Injury". The Journal of Neuroscience. 35 (16): 6517–6531. doi:10.1523/JNEUROSCI.5218-14.2015. PMC 6605214. PMID 25904802.
  7. ^ Lim J, Iyer A, Suen JY, Seow V, Reid RC, Brown L, et al. (February 2013). "C5aR and C3aR antagonists each inhibit diet-induced obesity, metabolic dysfunction, and adipocyte and macrophage signaling". FASEB Journal. 27 (2): 822–831. doi:10.1096/fj.12-220582. PMID 23118029. S2CID 25562647.
  8. ^ Markiewski MM, DeAngelis RA, Benencia F, Ricklin-Lichtsteiner SK, Koutoulaki A, Gerard C, et al. (November 2008). "Modulation of the antitumor immune response by complement". Nature Immunology. 9 (11): 1225–1235. doi:10.1038/ni.1655. PMC 2678913. PMID 18820683.
  9. ^ Wu KC, Condon ND, Hill TA, Reid RC, Fairlie D, Lim J (March 2023). "Ras related protein Rab5a regulates complement C5a receptor trafficking, chemotaxis and chemokine secretion in human macrophages". Journal of Innate Immunity. 15 (1): 468–484. doi:10.1159/000530012. PMC 10105068. PMID 36882040.
  10. ^ Feng Y, Zhao C, Deng Y, Wang H, Ma L, Liu S, et al. (April 2023). "Mechanism of activation and biased signaling in complement receptor C5aR1". Cell Research. 33 (4): 312–324. doi:10.1038/s41422-023-00779-2. PMC 9937529. PMID 36806352.
  11. ^ Li XX, Lee JD, Massey NL, Guan C, Robertson AA, Clark RJ, et al. (October 2020). "Pharmacological characterisation of small molecule C5aR1 inhibitors in human cells reveals biased activities for signalling and function". Biochemical Pharmacology. 180: 114156. doi:10.1016/j.bcp.2020.114156. PMID 32682759. S2CID 220653568.
  12. ^ Wang X, Iyer A, Lyons AB, Körner H, Wei W (2019). "Emerging Roles for G-protein Coupled Receptors in Development and Activation of Macrophages". Frontiers in Immunology. 10: 2031. doi:10.3389/fimmu.2019.02031. PMC 6718513. PMID 31507616.
  13. ^ Klos A, Wende E, Wareham KJ, Monk PN (January 2013). "International Union of Basic and Clinical Pharmacology. [corrected]. LXXXVII. Complement peptide C5a, C4a, and C3a receptors". Pharmacological Reviews. 65 (1): 500–543. doi:10.1124/pr.111.005223. PMID 23383423.
  14. ^ Gorman DM, Li XX, Lee JD, Fung JN, Cui CS, Lee HS, et al. (November 2021). "Development of Potent and Selective Agonists for Complement C5a Receptor 1 with In Vivo Activity". Journal of Medicinal Chemistry. 64 (22): 16598–16608. doi:10.1021/acs.jmedchem.1c01174. PMID 34762432. S2CID 244040645.
  15. ^ Wong AK, Finch AM, Pierens GK, Craik DJ, Taylor SM, Fairlie DP (August 1998). "Small molecular probes for G-protein-coupled C5a receptors: conformationally constrained antagonists derived from the C terminus of the human plasma protein C5a". Journal of Medicinal Chemistry. 41 (18): 3417–3425. doi:10.1021/jm9800651. PMID 9719594.
  16. ^ Gong Y, Barbay JK, Buntinx M, Li J, Wauwe JV, Claes C, et al. (July 2008). "Design and optimization of aniline-substituted tetrahydroquinoline C5a receptor antagonists". Bioorganic & Medicinal Chemistry Letters. 18 (14): 3852–3855. doi:10.1016/j.bmcl.2008.06.059. PMID 18595693.
  17. ^ Sumichika H, Sakata K, Sato N, Takeshita S, Ishibuchi S, Nakamura M, et al. (December 2002). "Identification of a potent and orally active non-peptide C5a receptor antagonist". The Journal of Biological Chemistry. 277 (51): 49403–49407. doi:10.1074/jbc.M209672200. PMID 12384495.
  18. ^ Seow V, Lim J, Cotterell AJ, Yau MK, Xu W, Lohman RJ, et al. (April 2016). "Receptor residence time trumps drug-likeness and oral bioavailability in determining efficacy of complement C5a antagonists". Scientific Reports. 6 (1): 24575. Bibcode:2016NatSR...624575S. doi:10.1038/srep24575. PMC 4837355. PMID 27094554.
  19. ^ Ulrich JT, Cieplak W, Paczkowski NJ, Taylor SM, Sanderson SD (May 2000). "Induction of an antigen-specific CTL response by a conformationally biased agonist of human C5a anaphylatoxin as a molecular adjuvant". Journal of Immunology. 164 (10): 5492–5498. doi:10.4049/jimmunol.164.10.5492. PMID 10799917. S2CID 38942679.

Further reading

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