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C5a1 receptor

Family: Complement peptide receptors

Contents:
Gene and Protein Information
Previous and Unofficial Names
Database Links
Agonists
Antagonists
Transduction Mechanisms
Tissue Distribution
Expression Datasets
Functional Assays
Physiological Functions
Physiological Consequences of Altering Gene Expression
Phenotypes, Alleles and Disease Models
Clinically-Relevant Mutations and Pathophysiology
General Comments
References
Gene and Protein Information
class A G protein-coupled receptor
Species TM AA Chromosomal Location Gene Symbol Gene Name Reference
Human 7 350 19q13.3-q13.4 C5AR1 complement component 5a receptor 1 32
Mouse 7 351 7 A1 C5ar1 complement component 5a receptor 1
Rat 7 352 1q12 C5ar1 complement component 5a receptor 1
Previous and Unofficial Names
C5aR1
CD88
C5R1
C5A
C5AR
complement component 5 receptor 1 (C5a ligand)
C5a anaphylatoxin chemotactic receptor
C5a-R
complement C5a receptor
complement component 5, receptor 1
complement component 5a receptor 1
D7Msu1
Database Links
ChEMBL Target 12679 (Hs), 101549 (Rn)
Ensembl ENSG00000197405 (Hs), ENSMUSG00000049130 (Mm), ENSRNOG00000047800 (Rn)
Entrez Gene 728 (Hs), 12273 (Mm), 113959 (Rn)
GeneCards C5AR1 (Hs)
GenitoUrinary Development Molecular Anatomy Project C5ar1 (Mm)
HomoloGene 20413 (Hs)
Human Protein Reference Database 00224 (Hs)
InterPro P21730 (Hs), Q3TZ86 (Mm), P97520 (Rn)
KEGG Gene hsa:728 (Hs), mmu:12273 (Mm), rno:113959 (Rn)
OMIM 113995 (Hs)
PharmGKB Gene PA25920 (Hs)
PhosphoSitePlus P21730 (Hs), P30993 (Mm), P97520 (Rn)
Protein Ontology (PRO) PRO:000001173 (Hs)
RefSeq Nucleotide NM_001736 (Hs), NM_007577 (Mm), NM_053619 (Rn)
RefSeq Protein NP_001727 (Hs), NP_031603 (Mm), NP_446071 (Rn)
TreeFam ENSG00000197405 (Hs), ENSMUSG00000049130 (Mm), ENSRNOG00000047800 (Rn)
UniGene Hs. 2161 (Hs)
UniProt P21730 (Hs), Q3TZ86 (Mm), P97520 (Rn)
Wikipedia C5a1 receptor
Complement peptide receptors
Search for 3D structures on the PDB
Search by keyword: Complement peptide receptors C5a1 receptor Search by accession number: P97520, P21730, Q3TZ86
Natural/Endogenous Ligand(s)
C3a {Sp: Human} , C3a {Sp: Mouse} , C3a {Sp: Rat}
C5a {Sp: Human} , C5a {Sp: Mouse} , C5a {Sp: Rat}
Comments: C5a anaphylatoxin has a higher potency than C3a anaphylatoxin
Rank order of potency (Human)
C5a, C5a des-Arg > C3a  [2]
Agonists
Key to terms and symbols Click column headers to sort
Ligand Sp. Action Affinity Units Reference
[125I]C5a (human) Hs Full agonist 8.7 pKd 43
C5a {Sp: Human} Hs Full agonist 8.0 – 9.0 pEC50 64,70
YSFKPMPLaR Hs Agonist 5.5 pEC50 102
C5a {Sp: Human} Hs Full agonist 9.1 – 9.2 pIC50 37,70
N-methyl-Phe-Lys-Pro-D-Cha-Cha-D-Arg-CO2H Hs Full agonist 7.6 pIC50 48,50
C5a des-Arg {Sp: Human} Hs Partial agonist 6.2 – 6.4 pIC50 11,37
YSFKPMPLaR Hs Full agonist 5.4 – 6.7 pIC50 25
Agonist Comments
YSFKPMPLaR is an agonist of both C5aR and C3aR. In addition to human cells it has been shown to have agonist actions in mice and rats [82,102]. RP S19 is an endogenous ribosomal protein, in the dimerised form it acts as an agonist of C5aR, however the referenced study [64] used recombinant protein. RP S19 gave a maximal reponse in a leukocyte chemotaxis assay at a concentration of 1nM [64]. Skp is a bacterial chaperone protein. IC50 values for agonists are derived from radioligand displacement assays.
Antagonists
Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Affinity Units Reference
CHIPS Hs Antagonist 9.0 pKd 72
W54011 Hs Antagonist 8.7 pKi 85
NDT9520492 Hs Antagonist 7.5 pKi 93
AcPhe-Orn-Pro-D-Cha-Trp-Arg Hs Antagonist 7.9 pIC50 96
A8Δ71-73 Mm Antagonist 7.57 pIC50 69
PMX205 Hs Antagonist 7.51 pIC50 57
PMX53 Hs Antagonist 7.1 – 7.7 pIC50 57,102
N-methyl-Phe-Lys-Pro-D-Cha-Trp-D-Arg-CO2H Hs Antagonist 7.2 pIC50 50
JPE1375 Hs Antagonist 7.0 pIC50 77
C089 Hs Antagonist 6.7 pIC50 50
RPR121154 Hs Antagonist 6.1 pIC50 6
L-156,602 Hs Antagonist 5.7 pIC50 90
View species-specific antagonist tables
Antagonist Comments
PMX53 is widely used as an parenterally- and orally-active antagonist of C5aR in mice and rats [73]. Although it has been demonstrated to block C5a binding in rat neutrophils (IC50 - 40nM), it does not inhibit C5a binding in murine cells [102]. However, it has specific C5aR antagonistic activity in vivo as demonstrated through comparisons with C5aR knockout mice [13]. PMX205 is also parenterally- and orally-active [73], but with greater lipophicity, and blood brain barrier penetrance than PMX53 [99-100]. PMX205 was also shown to be ineffective in C5aR knockout mice [46]. JPE1375 inhibits the chemotaxis of murine J774A.1 cells, but exhibits a reduced potency when compared to human neutrophils (IC50 - 420nM) [77]. A8 binds both C5aR and C5L2 with similar affinity, although the antagonistic properties of A8 at C5L2 remain untested [69]. In addition, other biologically relevant inhibitors of C5aR have been described. Chemotaxis inhibitory protein of S. aureus (CHIPS) is a 14.1 kDa antagonist of C5aR encoded on a bacteriophage. It has been demonstrated to have selective antagonistic properties against human C5aR in the micromolar concentration range [17].
Primary Transduction Mechanisms
Transducer Effector/Response
Gi/Go family
G protein (identity unknown) 		Phospholipase C stimulation
Other - See Comments
Comments:  Studies of C5aR signalling have determined cell-specific activation of downstream pathways. For instance, in macrophages C5aR signals via protein kinase C (PKC) δ to induce NFκB activation and translocation to the nucleus, whereas in neutrophils C5aR induces activation of IκB, the NFκB inhibitor [34]. Additionally, activated C5aR has also been shown to associate with Wiskott-Aldrich Syndrom Protein (WASP), a regulator of Rho-GTPases and therefore, cytoskeletal turnover [88]. In mesenchymal stem cells C5a induces a chemotaxis that is pertussis toxin sensitive, indicating a Gi mediated response, and signalling via MAPK and Akt pathways [78]. C5aR has also been demonstrated to cause transactivation of the epidermal growth factor (EGF) receptor in human umbilical vein endothelial cells [79].
References:  83
Secondary Transduction Mechanisms
Transducer Effector/Response
Gq/G11 family Phospholipase C stimulation
References:  54
Tissue Distribution
Mast cell subsets.
Species:  Human
Technique:  Immunocytochemistry.
References:  68
Cardiomyocytes
Species:  Human
Technique:  Northern blot
References:  35,95
Connective Tissue (synoviocytes, articular chondrocytes)
Species:  Human
Technique:  RT-PCR, immunocytochemistry
References:  67,104
Central Nervous System (astrocytes, microglia, neuron, neural stem cells, oligodendrocytes)
Species:  Human
Technique:  Immunohistochemistry
References:  31
Lung
Species:  Human
Technique:  Immunohistochemistry
References:  35
Liver
Species:  Human
Technique:  Northern blot
References:  35
Myeloid Leukocytes (neutrophil, eosinophil, basophil, monocytes)
Species:  Human
Technique:  Immunohistochemistry
References:  39,84
Vascular endothelial cells
Species:  Human
Technique:  Immunohistochemistry
References:  35
Vascular smooth muscle
Species:  Human
Technique:  Immunohistochemistry
References:  35,70
Eye (retinal pigment epithelial cells)
Species:  Human
Technique:  Flow cytometry
References:  29
Kidney
Species:  Human
Technique:  Immunohistochemistry
References:  31,63,66,74
Microvascular endothelial cells.
Species:  Mouse
Technique:  Radioligand binding.
References:  53
Central Nervous System (astrocytes, microglia, neuron, neural stem cells, oligodendrocytes)
Species:  Mouse
Technique:  Immunohistochemistry
References:  63,66,74
Central Nervous System (astrocytes, microglia, neuron, neural stem cells, oligodendrocytes)
Species:  Rat
Technique:  Immunohistochemistry
References:  63,66,74
Oligodendrocytes.
Species:  Rat
Technique:  RT-PCR.
References:  63
Tissue Distribution Comments
C5a1 was not found in pulmonary, hepatic, and intestinal epithelial cells, or lymphocytes in humans when examined with immunohistochemistry [22-23]. Although it has been previously reported that lymphocytes do not express C5aR, Lalli and colleagues (2008)[52] demonstrated a role for C5aR in T-cell survival. The techniques employed involved the use of a C5aR knockout mouse and a C5aR antagonist, to infer a function for C5aR on T-cells. No direct expression of either C5aR transcript or protein was demonstrated in this study. In addition, a recent study describing a GFP knock-in mouse, under the control of the C5aR promotor, failed to show GFP expression in either naïve or activated T-lymphocytes [20].
Expression Datasets

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Log average relative transcript abundance in mouse tissues measured by qPCR from Regard, J.B., Sato, I.T., and Coughlin, S.R. (2008). Anatomical profiling of G protein-coupled receptor expression. Cell, 135(3): 561-71. [PMID:18984166] [Raw data: website]

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Functional Assays
Chemotaxis
Species:  Human
Tissue:  Granulocytes, monocytes, RBL-2H3 C5aR transfected cells
Response measured:  Migration of cells up concentration gradient
References:  15,19,70,78
Intracellular calcium release
Species:  Human
Tissue:  Neutrophils, monocytes, HMC-1 cells, U937 cells, Rat hippocampal neurons
Response measured:  Transient increase in intracellular calcium concentrations upon receptor activation.
References:  65-66
Smooth muscle contraction
Species:  Human
Tissue:  Human umbilical artery
Response measured:  Contraction of smooth muscle
References:  12,70
ERK1/2 phosphorylation
Species:  Human
Tissue:  Mesenchymal stem cell, C5aR-transfected CHO cells, neutrophils
Response measured:  Increase in Phospho-ERK1/2 by Western blot
References:  75,78,87
Enzyme Release/Degranulation
Species:  Human
Tissue:  Neutrophils, RBL-2H3 C5aR transfected cells
Response measured:  Increase in myeloperoxidase, hydrogen peroxide (?peroxidase) and b-hexosaminidase release
References:  41,59,70
Measurement of degranulation in rat basophilic leukaemia cells transfected with the human C5a receptor.
Species:  Human
Tissue:  Rat basophilic leukaemia cells.
Response measured:  Degranulation.
References:  38
Physiological Functions
Chemotaxis.
Species:  Human
Tissue:  Granulocyte.
References:  60
Hepatocyte growth factor.
Species:  Rat
Tissue:  Liver.
References:  16
MAP kinase activation.
Species:  Mouse
Tissue:  Pituitary.
References:  28
Chemotaxis.
Species:  Human
Tissue:  Lymphocyte subsets.
References:  51
NF-κB activation.
Species:  Human
Tissue:  Neurons.
References:  66
Chemotaxis
Species:  Human
Tissue:  T cells, mesenchymal stem cells, dermal microvascular endothelial cells
References:  62,78
Apoptosis under oxygen/glucose deprivation
Species:  Mouse
Tissue:  Cortical neurons
References:  71
Chemokine (CCL2, CXCL2) release
Species:  Mouse
Tissue:  Microvascular endothelial cells
References:  53
Chemokine (IL-8) release
Species:  Human
Tissue:  Epithelial cells (lung, eye)
References:  29,35
Neutrophil extravasation
Species:  Mouse
Tissue:  Brain
References:  80
Neutropaenia
Species:  Rat
Tissue:  Blood
References:  81
Cell survival
Species:  Human
Tissue:  T-Lymphocytes
References:  52
Proliferation
Species:  Rat
Tissue:  Cerebellar granular neurons
References:  10
Histamine release
Species:  Human
Tissue:  Mast cells, basophils
References:  30
Degranulation
Species:  Human
Tissue:  Neutrophils, mast cells
References:  36,41,70
Physiological Consequences of Altering Gene Expression
Human C5a receptor knock-in mice facilitate the production and assessment of anti-inflammatory monoclonal antibodies.
Species:  Mouse
Tissue: 
Technique:  Transgenesis.
References:  55
Adenovirus-mediated in vivo silencing of the C5a receptor.
Species:  Mouse
Tissue: 
Technique:  RNA interference.
References:  86
Mice with receptor knockout exhibit increased susceptibility and lethality to Pseudomonas aeruginosa infection.
Species:  Mouse
Tissue:  Lung
Technique:  Gene knockouts
References:  45
Phenotypes, Alleles and Disease Models Mouse data from MGI

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Allele Composition & genetic background Accession Phenotype Id Phenotype Reference
C5ar1tm1Cge C5ar1tm1Cge/C5ar1tm1Cge
involves: 129S4/SvJae		 MGI:88232  MP:0001800 abnormal humoral immune response PMID: 8781237 
C5ar1tm1Cge C5ar1tm1Cge/C5ar1tm1Cge
involves: 129S4/SvJae		 MGI:88232  MP:0008719 impaired neutrophil recruitment PMID: 8779720 
C5ar1tm1Cge C5ar1tm1Cge/C5ar1tm1Cge
involves: 129S4/SvJae		 MGI:88232  MP:0009763 increased sensitivity to induced morbidity/mortality PMID: 8779720 
C5ar1tm1Raw C5ar1tm1Raw/C5ar1tm1Raw
B6.Cg-C5ar1		 MGI:88232  MP:0008481 increased spleen germinal center number PMID: 18455242 
C5ar1tm1Cge C5ar1tm1Cge/C5ar1tm1Cge
involves: 129S4/SvJae		 MGI:88232  MP:0002412 increased susceptibility to bacterial infection PMID: 8779720 
Clinically-Relevant Mutations and Pathophysiology
Disease:  Possible association with Henoch-Schonlein Purpura
References: 
Click column headers to sort
Type Species Molecular location Description Reference
Other Human nucleotide position 450 21
Disease:  Sepsis
Role:  C5aR blocking antibody-treated or C5aR-/- mice, increased survival and decreased serum proinflammatory cytokines in the caecal ligation and puncture model of sepsis. C5aR blocking antibody also reduces bacteraemia, as measure by bacterial colony forming units in blood, this is likely due to an impairment of neutrophil phagocytic activity in the presence of high C5a concentrations.
References:  14,40,42,76
Mutations not determined
Disease:  Inflammatory bowel disease
Role:  C5aR has been shown to be an aggrevating factor in acute models of IBD. In a rat model of TNBS induced colitis, treatment with the C5aR antagonist, PMX53, reduced pathology and mortality. Similarly, in a dextran sulphate-induced colitis mouse model, C5aR knockout mice are protected from acute pathology. However, in chronic colitis, the pathology of C5aR-deficient mice worsens.
References:  47,97
Mutations not determined
Disease:  Rheumatoid arthritis
Role:  In a rat model of antigen-induced monoarticular rheumatoid arthritis, oral administration of the C5aR antagonist PMX53 reduced oedema, inflammatory infiltrate and interarticular cytokines. However, in a double-blind, placebo controlled clinical trial, orally-administered PMX53 did not reduce synovial inflammation in rheumatoid arthritis patients.
References:  92,101
Mutations not determined
Disease:  Antiphospholipid syndrome
Role:  Antiphospholipid syndrome, C5aR functions as the activating receptor for neutrophils in antiphospholipid syndrome, neutrophil activation leads to the oxidative damage and pregancy loss characteristic of aPLS. Mice deficient in C5, or pharmacological blockage of C5aR, exhibit increased foetal growth and decreased foetal loss in aPLS.
References:  33,94
Mutations not determined
Disease:  Psoriasis
Role:  Evidence of a role for C5aR in psoriasis stems from the observation that the ligands for C5aR, C5a/C5a-des-arg, are the most abundant cytokine isolated from human psoriatic scales.
References:  9,61
Mutations not determined
Disease:  Neurodegenerative diseases, Alzheimer's disease
Role:  C5aR colocalises to microglia in amyloid plaques in the Tg2576 and hAPP mouse models of Alzheimer's disease. Inhbition of C5aR, through oral administration of PMX205, in these models reduces pathology and results in improved behavioural responses. Amylotrophic Lateral Sclerosis, In both the SODG93A and NFL-/- mouse models of ALS, C5aR is upregulated. The upregulation occurs in the presymptomatic stages of the NFL-/- model and the author observed this upregulation within motor neurons. However, in the SODG93A model, there is no early upregulation of C5aR within motor neurons, the upregulation occurs in the end stages of the model within motor neurons and astrocytes. The link between C5aR upregulation and ALS pathology has only been confirmed in the SODG93A model, where blockade of C5aR signalling with orally administered PMX205 increased survival and motor performance. Huntington's disease, In a rat model of 3-nitropropionic acid-induced Huntington's disease, C5aR inhibition via oral administration of either PMX53 or PMX205 reduced the behavioural phenotype and striatal lesions histologically. A decrease in striatal astrocytosis was also demonstrated, however whether this was a cause or effect of the reduction in striatal lesions was not investigated.
References:  1,24,27,44,98-99
Mutations not determined
Disease:  Ischaemic Reperfusion injury
Role:  The role of C5aR has been well studied in ischaemia/reperfusion (IR) injury. C5aR has been demonstrated to play a proinflammatory role, contributing to pathology, in IR injury of the heart, kidney, liver, intestine, and brain.
References:  3-5,18,26,56,91,103,105
Mutations not determined
Disease:  Injury aggravation in neurotrauma
Role:  in a mouse model of neurotrauma, invoked by the application of a liquid nitrogen cooled probe to the skull, C5aR has been demonstrated to be a key factor in injury aggravation. The authors attribute the attenuation of injury in both mice treated with the C5aR antagonist, PMX53, and mice deficient in C5, to a reduced neutrophil infiltration of the brain tissue post-injury. By contrast, in a rat model of spinal cord contusion injury, C5aR inhibition with PMX53 worsended injury outcomes.
References:  8,80
Mutations not determined
Clinically-Relevant Mutations and Pathophysiology Comments
The reported association of a C5aR polymorphism with Henoch-Schonlein purpura occurred in a population of patients with familial mediterranean fever. The C/T polymorphism is at base 450 in the coding sequence of C5aR. The association was noted, but the population size was insufficient to draw definitive conclusions [21]. Two other C5aR polymorphisms have been described but have no observable phenotype [7,89].
General Comments
Although C5aR is typically associated with the innate immune system, recently research on the receptor has elucidated novel roles. C5aR has been demonstrated on adult neural progenitor cells [74], mesenchymal stem cells [78] and perhaps has roles regulating the cell cycle in types of cancer [49,58].

REFERENCES

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1. Ager, RR; Fonseca, MI; Chu, SH; Sanderson, SD; Taylor, SM; Woodruff, TM; Tenner, AJ. (2010) Microglial C5aR (CD88) expression correlates with amyloid-beta deposition in murine models of Alzheimer's disease. J. Neurochem., 113 (2): 389-401. [PMID:20132482]

2. Ames, RS; Nuthulaganti, P; Kumar, C. (1996) In Xenopus oocytes the human C3a and C5a receptors elicit a promiscuous response to the anaphylatoxins. FEBS Lett., 395 (2-3): 157-9. [PMID:8898085]

3. Arumugam, TV; Shiels, IA; Strachan, AJ; Abbenante, G; Fairlie, DP; Taylor, SM. (2003) A small molecule C5a receptor antagonist protects kidneys from ischemia/reperfusion injury in rats. Kidney Int., 63 (1): 134-42. [PMID:12472776]

4. Arumugam, TV; Woodruff, TM; Lathia, JD; Selvaraj, PK; Mattson, MP; Taylor, SM. (2009) Neuroprotection in stroke by complement inhibition and immunoglobulin therapy. Neuroscience, 158 (3): 1074-89. [PMID:18691639]

5. Arumugam, TV; Woodruff, TM; Stocks, SZ; Proctor, LM; Pollitt, S; Shiels, IA; Reid, RC; Fairlie, DP; Taylor, SM. (2004) Protective effect of a human C5a receptor antagonist against hepatic ischaemia-reperfusion injury in rats. J. Hepatol., 40 (6): 934-41. [PMID:15158333]

6. Astles, PC; Brown, TJ; Cox, P; Halley, F; Lockey, PM; Mccarthy, C et al. (1997) New non-peptide C5a receptor antagonists. Bioorg Med Chem Lett., 7 (77): 907-912.

7. Barnes, KC; Caraballo, L; Muñoz, M; Zambelli-Weiner, A; Ehrlich, E; Burki, M; Jimenez, S; Mathias, RA; Stockton, ML; Deindl, P; et al.. (2004) A novel promoter polymorphism in the gene encoding complement component 5 receptor 1 on chromosome 19q13.3 is not associated with asthma and atopy in three independent populations. Clin. Exp. Allergy, 34 (5): 736-44. [PMID:15144465]

8. Beck, KD; Nguyen, HX; Galvan, MD; Salazar, DL; Woodruff, TM; Anderson, AJ. (2010) Quantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in the acute to chronic environment. Brain, 133 (Pt 2): 433-47. [PMID:20085927]

9. Bergh, K; Iversen, OJ; Lysvand, H. (1993) Surprisingly high levels of anaphylatoxin C5a des Arg are extractable from psoriatic scales. Arch. Dermatol. Res., 285 (3): 131-4. [PMID:8503693]

10. Bénard, M; Raoult, E; Vaudry, D; Leprince, J; Falluel-Morel, A; Gonzalez, BJ; Galas, L; Vaudry, H; Fontaine, M. (2008) Role of complement anaphylatoxin receptors (C3aR, C5aR) in the development of the rat cerebellum. Mol. Immunol., 45 (14): 3767-74. [PMID:18635264]

11. 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. [PMID:11773063]

12. Cochrane, CG; Müller-Eberhard, HJ. (1968) The derivation of two distinct anaphylatoxin activities from the third and fifth components of human complement. J. Exp. Med., 127 (2): 371-86. [PMID:4383923]

13. Costantini, K.J., Coulthard, L.G.J., Lor, M., Woodruff, T.M., Callaway, L.K., Finnell, R.H. and Taylor, S.M. (2010) C5aR protects against folate-deficiency induced neural tube defects in mice. Molecular Immunology, 47 (13): 2254.

14. Czermak, BJ; Sarma, V; Pierson, CL; Warner, RL; Huber-Lang, M; Bless, NM; Schmal, H; Friedl, HP; Ward, PA. (1999) Protective effects of C5a blockade in sepsis. Nat. Med., 5 (7): 788-92. [PMID:10395324]

15. Daffern, PJ; Pfeifer, PH; Ember, JA; Hugli, TE. (1995) C3a is a chemotaxin for human eosinophils but not for neutrophils. I. C3a stimulation of neutrophils is secondary to eosinophil activation. J. Exp. Med., 181 (6): 2119-27. [PMID:7760001]

16. Daveau, M; Benard, M; Scotte, M; Schouft, MT; Hiron, M; Francois, A; Salier, JP; Fontaine, M. (2004) Expression of a functional C5a receptor in regenerating hepatocytes and its involvement in a proliferative signaling pathway in rat. J. Immunol., 173 (5): 3418-24. [PMID:15322206]

17. de Haas, CJ; Veldkamp, KE; Peschel, A; Weerkamp, F; Van Wamel, WJ; Heezius, EC; Poppelier, MJ; Van Kessel, KP; van Strijp, JA. (2004) Chemotaxis inhibitory protein of Staphylococcus aureus, a bacterial antiinflammatory agent. J. Exp. Med., 199 (5): 687-95. [PMID:14993252]

18. de Vries, B; Köhl, J; Leclercq, WK; Wolfs, TG; van Bijnen, AA; Heeringa, P; Buurman, WA. (2003) Complement factor C5a mediates renal ischemia-reperfusion injury independent from neutrophils. J. Immunol., 170 (7): 3883-9. [PMID:12646657]

19. Deuel, TF; Senior, RM; Huang, JS; Griffin, GL. (1982) Chemotaxis of monocytes and neutrophils to platelet-derived growth factor. J. Clin. Invest., 69 (4): 1046-9. [PMID:7076844]

20. Dunkelberger, J; Zhou, L; Miwa, T; Song, WC. (2012) C5aR expression in a novel GFP reporter gene knockin mouse: implications for the mechanism of action of C5aR signaling in T cell immunity. J. Immunol., 188 (8): 4032-42. [PMID:22430734]

21. Erken, E; Gunesacar, R; Ozer, HT. (2010) Investigation of C5a receptor gene 450 C/T polymorphism in Turkish patients with familial Mediterranean fever. Mol. Biol. Rep., 37 (1): 273-6. [PMID:19657723]

22. Fayyazi, A; Sandau, R; Duong, LQ; Götze, O; Radzun, HJ; Schweyer, S; Soruri, A; Zwirner, J. (1999) C5a receptor and interleukin-6 are expressed in tissue macrophages and stimulated keratinocytes but not in pulmonary and intestinal epithelial cells. Am. J. Pathol., 154 (2): 495-501. [PMID:10027407]

23. Fayyazi, A; Scheel, O; Werfel, T; Schweyer, S; Oppermann, M; Götze, O; Radzun, HJ; Zwirner, J. (2000) The C5a receptor is expressed in normal renal proximal tubular but not in normal pulmonary or hepatic epithelial cells. Immunology, 99 (1): 38-45. [PMID:10651939]

24. Ferraiuolo, L; Heath, PR; Holden, H; Kasher, P; Kirby, J; Shaw, PJ. (2007) Microarray analysis of the cellular pathways involved in the adaptation to and progression of motor neuron injury in the SOD1 G93A mouse model of familial ALS. J. Neurosci., 27 (34): 9201-19. [PMID:17715356]

25. Finch, AM; Vogen, SM; Sherman, SA; Kirnarsky, L; Taylor, SM; Sanderson, SD. (1997) Biologically active conformer of the effector region of human C5a and modulatory effects of N-terminal receptor binding determinants on activity. J. Med. Chem., 40 (6): 877-84. [PMID:9083476]

26. Fleming, SD; Mastellos, D; Karpel-Massler, G; Shea-Donohue, T; Lambris, JD; Tsokos, GC. (2003) C5a causes limited, polymorphonuclear cell-independent, mesenteric ischemia/reperfusion-induced injury. Clin. Immunol., 108 (3): 263-73. [PMID:14499250]

27. Fonseca, MI; Ager, RR; Chu, SH; Yazan, O; Sanderson, SD; LaFerla, FM; Taylor, SM; Woodruff, TM; Tenner, AJ. (2009) Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease. J. Immunol., 183 (2): 1375-83. [PMID:19561098]

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To cite this database page, please use the following:

Liam Coulthard, Owen Hawksworth, Trent Woodruff.
Complement peptide receptors: C5a1 receptor. Last modified on 28/02/2013. Accessed on 19/05/2013. IUPHAR database (IUPHAR-DB), http://www.iuphar-db.org/DATABASE/ObjectDisplayForward?objectId=32.


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