C3AR1
C3a anaphylatoxin chemotactic receptor
Also known as: AZ3B, C3AR, C3AR_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q16581
- Gene
- C3AR1
- Ensembl
- ENSG00000171860
- Chromosome
- 12
- Canonical length
- 482 aa
- Protein class
- G-protein coupled receptors, Predicted membrane proteins
OverviewNCBI Gene
C3a is an anaphylatoxin released during activation of the complement system. The protein encoded by this gene is an orphan G protein-coupled receptor for C3a. Binding of C3a by the encoded receptor activates chemotaxis, granule enzyme release, superoxide anion production, and bacterial opsonization. [provided by RefSeq, May 2016]
Canonical amino-acid sequenceUniProt
482 residues, UniProt reviewed canonical sequence.
>Q16581|C3AR1
1 MASFSAETNS TDLLSQPWNE PPVILSMVIL SLTFLLGLPG NGLVLWVAGL KMQRTVNTIW
61 FLHLTLADLL CCLSLPFSLA HLALQGQWPY GRFLCKLIPS IIVLNMFASV FLLTAISLDR
121 CLVVFKPIWC QNHRNVGMAC SICGCIWVVA FVMCIPVFVY REIFTTDNHN RCGYKFGLSS
181 SLDYPDFYGD PLENRSLENI VQPPGEMNDR LDPSSFQTND HPWTVPTVFQ PQTFQRPSAD
241 SLPRGSARLT SQNLYSNVFK PADVVSPKIP SGFPIEDHET SPLDNSDAFL STHLKLFPSA
301 SSNSFYESEL PQGFQDYYNL GQFTDDDQVP TPLVAITITR LVVGFLLPSV IMIACYSFIV
361 FRMQRGRFAK SQSKTFRVAV VVVAVFLVCW TPYHIFGVLS LLTDPETPLG KTLMSWDHVC
421 IALASANSCF NPFLYALLGK DFRKKARQSI QGILEAAFSE ELTRSTHCPS NNVISERNST
481 TVLocalizationUniProt · AlphaFold · HPA
Whether an antibody against C3AR1 can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Cell surface
- Secreted
- No
- Transmembrane segments
- 7
- Mean surface accessibility (rSASA)
- 0.43
- Highest tissue expression
- 38 nTPM
Expression across tissuesHPA
Tissue
- appendix: 38 nTPM
- bone marrow: 22 nTPM
- placenta: 21 nTPM
- adipose tissue: 17 nTPM
- lung: 16 nTPM
- gallbladder: 15 nTPM
Single-cell type
- neutrophils: 371 nCPM
- hofbauer cells: 283 nCPM
- kupffer cells: 222 nCPM
- monocytes: 218 nCPM
- macrophages: 206 nCPM
- neutrophil progenitors: 197 nCPM
Immune cell
- basophil: 903 nTPM
- eosinophil: 453 nTPM
- non-classical monocyte: 373 nTPM
- intermediate monocyte: 274 nTPM
- classical monocyte: 105 nTPM
- total PBMC: 76 nTPM
Brain region
- white matter: 32 nTPM
- medulla oblongata: 20 nTPM
- spinal cord: 17 nTPM
- thalamus: 16 nTPM
- pons: 15 nTPM
- hypothalamus: 14 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about C3AR1.
Disease | GeneticClinVar
1 pathogenic / likely-pathogenic of 82 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
ReferencesPubMed · IEDB
Publications for C3AR1 from three distinct lines of evidence, kept separate because they answer different questions: whether antibodies are directed at the protein, whether a B-cell epitope has been mapped on it, and whether a T-cell epitope has. Each is labelled with its source.
Reference: AutoantibodyPubMed
2 publications
- Low Concentrations of C5a Complement Receptor Antibodies Are Linked to Disease Activity and Relapse in Antineutrophil Cytoplasmic Autoantibody-Associated Vasculitis.
2023 · Arthritis Rheumatol · RCR 0.9 · 7 citations - The Influence of Anti-C3aR and Anti-C5aR Antibody Levels on the Course of Specific Glomerulonephritis Types.
2025 · J Clin Med
Sources: PubMed — antigen-level antibody evidence from a custom retrieval. Records matching a controlled set of autoantibody terms (the MeSH descriptors Autoantibodies and Autoantigens, with title and abstract term variants) were obtained through NCBI E-utilities, and their titles and abstracts parsed for constructions that direct an antibody at a named protein rather than for co-occurrence. Captured names were resolved against UniProt nomenclature and each antigen adjudicated individually against the source text. Bibliographic records from PubMed and MeSH, U.S. National Library of Medicine; citation metrics from NIH iCite (Hutchins et al., PLoS Biology 2016). Titles link to PubMed; abstracts are not reproduced here. The NLM does not endorse this analysis.
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 1.59
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.3
- DepMap mean gene effect
- 0
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- adenylate cyclase-inhibiting G protein-coupled receptor signaling pathway
- blood circulation
- calcium-mediated signaling
- chemotaxis
- complement receptor mediated signaling pathway
- G protein-coupled receptor signaling pathway
- inflammatory response
- phospholipase C-activating G protein-coupled receptor signaling pathway
- positive regulation of angiogenesis
- positive regulation of cytosolic calcium ion concentration
- positive regulation of macrophage chemotaxis
- positive regulation of neutrophil chemotaxis
- positive regulation of vascular endothelial growth factor production
Molecular functions
- complement component C5a receptor activity
- G protein-coupled receptor activity
- complement component C3a receptor activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of C3AR1 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads C3AR1 as an antibody target. Whether an autoantibody or antibody against C3AR1 could matter depends on whether native C3AR1 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
C3AR1 is annotated at the cell surface, where native C3AR1 is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.
Annotation status
The present source text does not explicitly label C3AR1 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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