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}}
{{Infobox_gene}}
{{Infobox_gene}}
'''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>.
'''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)]].


== Function ==
== Function ==


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.
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>

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>.


==References==
==References==
{{reflist}}
{{reflist}}

==Further reading==
{{refbegin | 2}}
*{{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 }}
*{{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 }}
*{{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 }}
*{{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 }}
*{{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 }}
*{{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}}
*{{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 }}
*{{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 }}
*{{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}}
*{{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 }}
*{{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 }}
{{refend}}


==External links==
==External links==

Revision as of 11:05, 15 February 2024

C5AR2
Identifiers
AliasesC5AR2, C5L2, GPR77, complement component 5a receptor 2, complement C5a receptor 2, C5a2
External IDsOMIM: 609949 MGI: 2442013 HomoloGene: 49549 GeneCards: C5AR2
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
View/Edit HumanView/Edit Mouse

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

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000134830Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000074361Ensembl, 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. ^ 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)
  6. ^ "HGNC:4527". Retrieved 2019-08-30.
  7. ^ 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)
  8. ^ 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)
  9. ^ 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.
  10. ^ 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)
  11. ^ 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)
  12. ^ 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.
  13. ^ 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)
  14. ^ 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.
  15. ^ 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)
  16. ^ 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)
  17. ^ 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.
  18. ^ 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)
  19. ^ 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

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