C5AR2: Difference between revisions
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{{Short description|Protein-coding gene in the species Homo sapiens}} |
{{Short description|Protein-coding gene in the species Homo sapiens}} |
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{{Infobox_gene}} |
{{Infobox_gene}} |
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'''C5a anaphylatoxin chemotactic receptor 2''' is a [[protein]] of the [[complement system]] that in humans is encoded by the ''C5AR2'' [[gene]] <ref name="pmid11165367">{{Cite journal |last=Ohno |first=Mitsuharu |last2=Hirata |first2=Tomohisa |last3=Enomoto |first3=Makoto |last4=Araki |first4=Takeyoshi |last5=Ishimaru |first5=Hiroshi |last6=Takahashi |first6=Tsuneo A. |date=2000-06 |title=A putative chemoattractant receptor, C5L2, is expressed in granulocyte and immature dendritic cells, but not in mature dendritic cells |url=https://linkinghub.elsevier.com/retrieve/pii/S0161589000000675 |journal=Molecular Immunology |language=en |volume=37 |issue=8 |pages=407–412 |doi=10.1016/S0161-5890(00)00067-5}}</ref><ref name="HGNC GPR77">{{cite web |title=HGNC:4527 |url=https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/4527 |access-date=2019-08-30}}</ref>. It is highly expressed in the blood and spleen <ref>{{Cite journal |last=Zhu |first=Yumeng |last2=Wang |first2=Xiaochao |last3=Xu |first3=Yanqing |last4=Chen |first4=Lu |last5=Ding |first5=Peipei |last6=Chen |first6=Jianfeng |last7=Hu |first7=Weiguo |date=2021-09-14 |title=An Integrated Analysis of C5AR2 Related to Malignant Properties and Immune Infiltration of Breast Cancer |url=https://www.frontiersin.org/articles/10.3389/fonc.2021.736725/full |journal=Frontiers in Oncology |volume=11 |doi=10.3389/fonc.2021.736725 |issn=2234-943X |pmc=PMC8476960 |pmid=34595119}}</ref>, predominantly by [[Myeloid tissue|myeloid]] cells <ref>{{Cite journal |last=Bamberg |first=Claire E. |last2=Mackay |first2=Charles R. |last3=Lee |first3=Hyun |last4=Zahra |first4=David |last5=Jackson |first5=Jenny |last6=Lim |first6=Yun Si |last7=Whitfeld |first7=Peter L. |last8=Craig |first8=Stewart |last9=Corsini |first9=Erin |last10=Lu |first10=Bao |last11=Gerard |first11=Craig |last12=Gerard |first12=Norma P. |date=2010-03 |title=The C5a Receptor (C5aR) C5L2 Is a Modulator of C5aR-mediated Signal Transduction |url=https://linkinghub.elsevier.com/retrieve/pii/S002192581958749X |journal=Journal of Biological Chemistry |language=en |volume=285 |issue=10 |pages=7633–7644 |doi=10.1074/jbc.M109.092106 |pmc=PMC2844210 |pmid=20044484}}</ref><ref>{{Cite journal |last=Karsten |first=Christian M. |last2=Wiese |first2=Anna V. |last3=Mey |first3=Fabian |last4=Figge |first4=Julia |last5=Woodruff |first5=Trent M. |last6=Reuter |first6=Tom |last7=Scurtu |first7=Olga |last8=Kordowski |first8=Anna |last9=Almeida |first9=Larissa N. |last10=Briukhovetska |first10=Daria |last11=Quell |first11=Katharina M. |last12=Sun |first12=Jing |last13=Ender |first13=Fanny |last14=Schmudde |first14=Inken |last15=Vollbrandt |first15=Tillman |date=2017-11-01 |title=Monitoring C5aR2 Expression Using a Floxed tdTomato-C5aR2 Knock-In Mouse |url=https://journals.aai.org/jimmunol/article/199/9/3234/109777/Monitoring-C5aR2-Expression-Using-a-Floxed |journal=The Journal of Immunology |language=en |volume=199 |issue=9 |pages=3234–3248 |doi=10.4049/jimmunol.1700710 |issn=0022-1767}}</ref>. |
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'''C5a anaphylatoxin chemotactic receptor 2''' is a [[protein]] that in humans is encoded by the ''C5AR2'' [[gene]].<ref name="pmid11165367">{{cite journal |vauthors=Lee DK, George SR, Cheng R, Nguyen T, Liu Y, Brown M, Lynch KR, O'Dowd BF | title = Identification of four novel human G protein-coupled receptors expressed in the brain | journal = Brain Res Mol Brain Res | volume = 86 | issue = 1–2 | pages = 13–22 |date=Feb 2001 | pmid = 11165367 | doi =10.1016/S0169-328X(00)00242-4 }}</ref><ref name="HGNC GPR77"/> It's a complement component [[G protein-coupled receptor]], of [[Rhodopsin-like receptors|class A (rhodopsin-like)]]. |
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== Function == |
== Function == |
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The [[anaphylatoxin]]s [[C3a (complement)|C3a]] and [[Complement component 5a|C5a]] are fragments of [[Complement component 3|C3]] and [[Complement component 5|C5]] generated via [[Proteolysis|proteolytic cleavage]] by [[C3-convertase|C3 convertases]] and [[C5-convertase|C5 convertases]] during the complement cascade. They are potent pro-inflammatory mediators which bind to the [[anaphylatoxin receptors]], [[C3a receptor|C3aR]], [[C5a receptor|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 mediates a broad range of effects in host defense, including [[Chemotaxis|chemoattraction]], [[vasodilation]] and immune cell activation <ref>{{Cite journal |last=Klos |first=Andreas |last2=Tenner |first2=Andrea J. |last3=Johswich |first3=Kay-Ole |last4=Ager |first4=Rahasson R. |last5=Reis |first5=Edimara S. |last6=Köhl |first6=Jörg |date=2009-09-01 |title=The role of the anaphylatoxins in health and disease |url=https://www.sciencedirect.com/science/article/pii/S0161589009001965 |journal=Molecular Immunology |series=12th European Meeting on Complement in Human Disease |volume=46 |issue=14 |pages=2753–2766 |doi=10.1016/j.molimm.2009.04.027 |issn=0161-5890 |pmc=PMC2725201 |pmid=19477527}}</ref>. C5aR2 binds C5a, but lacks GPCR activity <ref name=":0">{{Cite journal |last=Scola |first=Anne-Marie |last2=Johswich |first2=Kay-Ole |last3=Morgan |first3=B. Paul |last4=Klos |first4=Andreas |last5=Monk |first5=Peter N. |date=2009-03 |title=The human complement fragment receptor, C5L2, is a recycling decoy receptor |url=https://linkinghub.elsevier.com/retrieve/pii/S0161589008007499 |journal=Molecular Immunology |language=en |volume=46 |issue=6 |pages=1149–1162 |doi=10.1016/j.molimm.2008.11.001 |pmc=PMC2697321 |pmid=19100624}}</ref>, and its function is less well understood. |
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The [[anaphylatoxin]]s [[C3a (complement)|C3a]], [[C4a]], and [[Complement component 5a|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 [[neutrophil]]s and may modulate C5a1 activity.<ref name="HGNC GPR77">{{cite web | title = HGNC:4527 | url = https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/4527| access-date =2019-08-30 }}</ref><ref name="pmid16204243">{{cite journal |vauthors=Gerard NP, Lu B, Liu P, Craig S, Fujiwara Y, Okinaga S, Gerard C | title = An anti-inflammatory function for the complement anaphylatoxin C5a-binding protein, C5L2 | journal = J. Biol. Chem. | volume = 280 | issue = 48 | pages = 39677–80 |date=December 2005 | pmid = 16204243 | doi = 10.1074/jbc.C500287200 | doi-access = free }}</ref> |
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C5aR2 was initially thought be a [[Decoy receptors|decoy receptor]], acting as a sink for C5a to negatively regulate C5aR1 function <ref name=":0" />. However, more recent research has uncovered independent roles for C5aR2, including modulation of the innate immune response in myeloid cells <ref>{{Cite journal |last=Li |first=Xaria X. |last2=Clark |first2=Richard J. |last3=Woodruff |first3=Trent M. |date=2020-08-15 |title=C5aR2 Activation Broadly Modulates the Signaling and Function of Primary Human Macrophages |url=https://journals.aai.org/jimmunol/article/205/4/1102/110215/C5aR2-Activation-Broadly-Modulates-the-Signaling |journal=The Journal of Immunology |language=en |volume=205 |issue=4 |pages=1102–1112 |doi=10.4049/jimmunol.2000407 |issn=0022-1767}}</ref><ref>{{Cite journal |last=Wright |first=Oliver |last2=Harris |first2=Anna |last3=Nguyen |first3=Van Dien |last4=Zhou |first4=You |last5=Durand |first5=Maxim |last6=Jayyaratnam |first6=Abbie |last7=Gormley |first7=Darren |last8=O’Neill |first8=Luke A. J. |last9=Triantafilou |first9=Kathy |last10=Nichols |first10=Eva Maria |last11=Booty |first11=Lee M. |date=2023-11-25 |title=C5aR2 Regulates STING-Mediated Interferon Beta Production in Human Macrophages |url=https://www.mdpi.com/2073-4409/12/23/2707 |journal=Cells |language=en |volume=12 |issue=23 |pages=2707 |doi=10.3390/cells12232707 |issn=2073-4409 |pmc=PMC10706378 |pmid=38067135}}</ref>, translocation of C5a to drive [[Chemotaxis|transendothelial migration]] of [[Neutrophil|neutrophils]] <ref>{{Cite journal |last=Miyabe |first=Yoshishige |last2=Miyabe |first2=Chie |last3=Mani |first3=Vinidhra |last4=Mempel |first4=Thorsten R. |last5=Luster |first5=Andrew D. |date=2019-05-24 |title=Atypical complement receptor C5aR2 transports C5a to initiate neutrophil adhesion and inflammation |url=https://www.science.org/doi/10.1126/sciimmunol.aav5951 |journal=Science Immunology |language=en |volume=4 |issue=35 |doi=10.1126/sciimmunol.aav5951 |issn=2470-9468}}</ref>, [[Arrestin beta 2|β-arrestin]] recruitment and modulation of [[MAPK/ERK pathway|ERK signalling]] <ref>{{Cite journal |last=Croker |first=Daniel E |last2=Monk |first2=Peter N |last3=Halai |first3=Reena |last4=Kaeslin |first4=Geraldine |last5=Schofield |first5=Zoe |last6=Wu |first6=Mike CL |last7=Clark |first7=Richard J |last8=Blaskovich |first8=Mark AT |last9=Morikis |first9=Dimitrios |last10=Floudas |first10=Christodoulos A |last11=Cooper |first11=Matthew A |last12=Woodruff |first12=Trent M |date=2016-09 |title=Discovery of functionally selective C5aR2 ligands: novel modulators of C5a signalling |url=https://onlinelibrary.wiley.com/doi/10.1038/icb.2016.43 |journal=Immunology & Cell Biology |language=en |volume=94 |issue=8 |pages=787–795 |doi=10.1038/icb.2016.43 |issn=0818-9641}}</ref><ref>{{Cite journal |last=Croker |first=Daniel E |last2=Halai |first2=Reena |last3=Kaeslin |first3=Geraldine |last4=Wende |first4=Elisabeth |last5=Fehlhaber |first5=Beate |last6=Klos |first6=Andreas |last7=Monk |first7=Peter N |last8=Cooper |first8=Matthew A |date=2014-08 |title=C5a2 can modulate ERK1/2 signaling in macrophages via heteromer formation with C5a1 and β‐arrestin recruitment |url=https://onlinelibrary.wiley.com/doi/10.1038/icb.2014.32 |journal=Immunology & Cell Biology |language=en |volume=92 |issue=7 |pages=631–639 |doi=10.1038/icb.2014.32 |issn=0818-9641}}</ref> and modulation of [[lipid metabolism]] in [[obesity]] through [[Acylation stimulating protein|C3a-desArg]] binding <ref>{{Cite journal |last=Fisette |first=Alexandre |last2=Cianflone |first2=Katherine |date=2010-06-01 |title=The ASP and C5L2 pathway: another bridge between inflammation and metabolic homeostasis |url=https://www.tandfonline.com/doi/full/10.2217/clp.10.21 |journal=Clinical Lipidology |language=en |volume=5 |issue=3 |pages=367–377 |doi=10.2217/clp.10.21 |issn=1758-4299}}</ref>. C5aR2 has been implicated in a broad range of inflammatory and infectious diseases <ref>{{Cite journal |last=Li |first=Rui |last2=Coulthard |first2=Liam G. |last3=Wu |first3=M. C. L. |last4=Taylor |first4=Stephen M. |last5=Woodruff |first5=Trent M. |date=2013-03 |title=C5L2: a controversial receptor of complement anaphylatoxin, C5a |url=https://onlinelibrary.wiley.com/doi/abs/10.1096/fj.12-220509 |journal=The FASEB Journal |language=en |volume=27 |issue=3 |pages=855–864 |doi=10.1096/fj.12-220509 |issn=0892-6638}}</ref><ref>{{Cite journal |last=Li |first=Xaria X. |last2=Lee |first2=John D. |last3=Kemper |first3=Claudia |last4=Woodruff |first4=Trent M. |date=2019-06-15 |title=The Complement Receptor C5aR2: A Powerful Modulator of Innate and Adaptive Immunity |url=https://doi.org/10.4049/jimmunol.1900371 |journal=The Journal of Immunology |volume=202 |issue=12 |pages=3339–3348 |doi=10.4049/jimmunol.1900371 |issn=0022-1767}}</ref>. |
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==References== |
==References== |
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{{reflist}} |
{{reflist}} |
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==Further reading== |
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{{refbegin | 2}} |
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*{{cite journal |vauthors=Klos A, Wende E, Wareham KJ, Monk PN |title=International Union of Pharmacology. LXXXVII. Complement peptide C5a, C4a, and C3a receptors |journal=Pharmacol. Rev. |volume=65 |issue= 1 |pages= 500–43 |year= 2013 |pmid= 23383423 |doi=10.1124/pr.111.005223|doi-access=free }} |
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*{{cite journal |vauthors=Ohno M, Hirata T, Enomoto M, etal |title=A putative chemoattractant receptor, C5L2, is expressed in granulocyte and immature dendritic cells, but not in mature dendritic cells |journal=Mol. Immunol. |volume=37 |issue= 8 |pages= 407–12 |year= 2000 |pmid= 11090875 |doi=10.1016/S0161-5890(00)00067-5 }} |
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*{{cite journal |vauthors=Cain SA, Monk PN |title=The orphan receptor C5L2 has high affinity binding sites for complement fragments C5a and C5a des-Arg(74) |journal=J. Biol. Chem. |volume=277 |issue= 9 |pages= 7165–9 |year= 2002 |pmid= 11773063 |doi= 10.1074/jbc.C100714200 |doi-access= free }} |
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*{{cite journal |vauthors=Strausberg RL, Feingold EA, Grouse LH, etal |title=Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 26 |pages= 16899–903 |year= 2003 |pmid= 12477932 |doi= 10.1073/pnas.242603899 | pmc=139241 |bibcode=2002PNAS...9916899M |doi-access=free }} |
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*{{cite journal |vauthors=Kalant D, Cain SA, Maslowska M, etal |title=The chemoattractant receptor-like protein C5L2 binds the C3a des-Arg77/acylation-stimulating protein |journal=J. Biol. Chem. |volume=278 |issue= 13 |pages= 11123–9 |year= 2003 |pmid= 12540846 |doi= 10.1074/jbc.M206169200 |doi-access=free }} |
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*{{cite journal |vauthors=Otto M, Hawlisch H, Monk PN, etal |title=C5a mutants are potent antagonists of the C5a receptor (CD88) and of C5L2: position 69 is the locus that determines agonism or antagonism |journal=J. Biol. Chem. |volume=279 |issue= 1 |pages= 142–51 |year= 2004 |pmid= 14570896 |doi= 10.1074/jbc.M310078200 |doi-access= free}} |
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*{{cite journal |vauthors=Gerhard DS, Wagner L, Feingold EA, etal |title=The Status, Quality, and Expansion of the NIH Full-Length cDNA Project: The Mammalian Gene Collection (MGC) |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121–7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504 | pmc=528928 }} |
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*{{cite journal |vauthors=Huber-Lang M, Sarma JV, Rittirsch D, etal |title=Changes in the novel orphan, C5a receptor (C5L2), during experimental sepsis and sepsis in humans |journal=J. Immunol. |volume=174 |issue= 2 |pages= 1104–10 |year= 2005 |pmid= 15634936 |doi= 10.4049/jimmunol.174.2.1104|doi-access=free }} |
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*{{cite journal |vauthors=Kalant D, MacLaren R, Cui W, etal |title=C5L2 is a functional receptor for acylation-stimulating protein |journal=J. Biol. Chem. |volume=280 |issue= 25 |pages= 23936–44 |year= 2005 |pmid= 15833747 |doi= 10.1074/jbc.M406921200 |doi-access= free}} |
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*{{cite journal |vauthors=Johswich K, Martin M, Thalmann J, etal |title=Ligand specificity of the anaphylatoxin C5L2 receptor and its regulation on myeloid and epithelial cell lines |journal=J. Biol. Chem. |volume=281 |issue= 51 |pages= 39088–95 |year= 2007 |pmid= 17068344 |doi= 10.1074/jbc.M609734200 |doi-access= free }} |
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*{{cite journal |vauthors=Scola AM, Higginbottom A, Partridge LJ, etal |title=The Role of the N-terminal Domain of the Complement Fragment Receptor C5L2 in Ligand Binding |journal=J. Biol. Chem. |volume=282 |issue= 6 |pages= 3664–71 |year= 2007 |pmid= 17158873 |doi= 10.1074/jbc.M609178200 | pmc=2873560 |doi-access=free }} |
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{{refend}} |
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==External links== |
==External links== |
Revision as of 11:05, 15 February 2024
C5a anaphylatoxin chemotactic 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].
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 potent 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 mediates 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
- ^ a b c GRCh38: Ensembl release 89: ENSG00000134830 – Ensembl, May 2017
- ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000074361 – Ensembl, May 2017
- ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ Ohno M, Hirata T, Enomoto M, Araki T, Ishimaru H, Takahashi TA (2000-06). "A putative chemoattractant receptor, C5L2, is expressed in granulocyte and immature dendritic cells, but not in mature dendritic cells". Molecular Immunology. 37 (8): 407–412. doi:10.1016/S0161-5890(00)00067-5.
{{cite journal}}
: Check date values in:|date=
(help) - ^ "HGNC:4527". Retrieved 2019-08-30.
- ^ Zhu Y, Wang X, Xu Y, Chen L, Ding P, Chen J, Hu W (2021-09-14). "An Integrated Analysis of C5AR2 Related to Malignant Properties and Immune Infiltration of Breast Cancer". Frontiers in Oncology. 11. doi:10.3389/fonc.2021.736725. ISSN 2234-943X. PMC 8476960. PMID 34595119.
{{cite journal}}
: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ Bamberg CE, Mackay CR, Lee H, Zahra D, Jackson J, Lim YS, Whitfeld PL, Craig S, Corsini E, Lu B, Gerard C, Gerard NP (2010-03). "The C5a Receptor (C5aR) C5L2 Is a Modulator of C5aR-mediated Signal Transduction". Journal of Biological Chemistry. 285 (10): 7633–7644. doi:10.1074/jbc.M109.092106. PMC 2844210. PMID 20044484.
{{cite journal}}
: Check date values in:|date=
(help)CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ Karsten CM, Wiese AV, Mey F, Figge J, Woodruff TM, Reuter T, Scurtu O, Kordowski A, Almeida LN, Briukhovetska D, Quell KM, Sun J, Ender F, Schmudde I, Vollbrandt T (2017-11-01). "Monitoring C5aR2 Expression Using a Floxed tdTomato-C5aR2 Knock-In Mouse". The Journal of Immunology. 199 (9): 3234–3248. doi:10.4049/jimmunol.1700710. ISSN 0022-1767.
- ^ Klos A, Tenner AJ, Johswich KO, Ager RR, Reis ES, Köhl J (2009-09-01). "The role of the anaphylatoxins in health and disease". Molecular Immunology. 12th European Meeting on Complement in Human Disease. 46 (14): 2753–2766. doi:10.1016/j.molimm.2009.04.027. ISSN 0161-5890. PMC 2725201. PMID 19477527.
{{cite journal}}
: CS1 maint: PMC format (link) - ^ a b Scola AM, Johswich KO, Morgan BP, Klos A, Monk PN (2009-03). "The human complement fragment receptor, C5L2, is a recycling decoy receptor". Molecular Immunology. 46 (6): 1149–1162. doi:10.1016/j.molimm.2008.11.001. PMC 2697321. PMID 19100624.
{{cite journal}}
: Check date values in:|date=
(help)CS1 maint: PMC format (link) - ^ Li XX, Clark RJ, Woodruff TM (2020-08-15). "C5aR2 Activation Broadly Modulates the Signaling and Function of Primary Human Macrophages". The Journal of Immunology. 205 (4): 1102–1112. doi:10.4049/jimmunol.2000407. ISSN 0022-1767.
- ^ Wright O, Harris A, Nguyen VD, Zhou Y, Durand M, Jayyaratnam A, Gormley D, O’Neill Luke A. J., Triantafilou K, Nichols EM, Booty LM (2023-11-25). "C5aR2 Regulates STING-Mediated Interferon Beta Production in Human Macrophages". Cells. 12 (23): 2707. doi:10.3390/cells12232707. ISSN 2073-4409. PMC 10706378. PMID 38067135.
{{cite journal}}
: Vancouver style error: non-Latin character in name 8 (help)CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ Miyabe Y, Miyabe C, Mani V, Mempel TR, Luster AD (2019-05-24). "Atypical complement receptor C5aR2 transports C5a to initiate neutrophil adhesion and inflammation". Science Immunology. 4 (35). doi:10.1126/sciimmunol.aav5951. ISSN 2470-9468.
- ^ Croker DE, Monk PN, Halai R, Kaeslin G, Schofield Z, Wu MC, Clark RJ, Blaskovich MA, Morikis D, Floudas CA, Cooper MA, Woodruff TM (2016-09). "Discovery of functionally selective C5aR2 ligands: novel modulators of C5a signalling". Immunology & Cell Biology. 94 (8): 787–795. doi:10.1038/icb.2016.43. ISSN 0818-9641.
{{cite journal}}
: Check date values in:|date=
(help) - ^ Croker DE, Halai R, Kaeslin G, Wende E, Fehlhaber B, Klos A, Monk PN, Cooper MA (2014-08). "C5a2 can modulate ERK1/2 signaling in macrophages via heteromer formation with C5a1 and β‐arrestin recruitment". Immunology & Cell Biology. 92 (7): 631–639. doi:10.1038/icb.2014.32. ISSN 0818-9641.
{{cite journal}}
: Check date values in:|date=
(help) - ^ Fisette A, Cianflone K (2010-06-01). "The ASP and C5L2 pathway: another bridge between inflammation and metabolic homeostasis". Clinical Lipidology. 5 (3): 367–377. doi:10.2217/clp.10.21. ISSN 1758-4299.
- ^ Li R, Coulthard LG, Wu MC, Taylor SM, Woodruff TM (2013-03). "C5L2: a controversial receptor of complement anaphylatoxin, C5a". The FASEB Journal. 27 (3): 855–864. doi:10.1096/fj.12-220509. ISSN 0892-6638.
{{cite journal}}
: Check date values in:|date=
(help)CS1 maint: unflagged free DOI (link) - ^ Li XX, Lee JD, Kemper C, Woodruff TM (2019-06-15). "The Complement Receptor C5aR2: A Powerful Modulator of Innate and Adaptive Immunity". The Journal of Immunology. 202 (12): 3339–3348. doi:10.4049/jimmunol.1900371. ISSN 0022-1767.
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.