IFNAR1
Interferon alpha/beta receptor 1
Also known as: IFNAR, IFRC, INAR1_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P17181
- Gene
- IFNAR1
- Ensembl
- ENSG00000142166
- Chromosome
- 21
- Canonical length
- 557 aa
- Protein class
- Cancer-related genes, Disease related genes, FDA approved drug targets, Plasma proteins, Predicted intracellular proteins, Predicted membrane proteins, Transporters
OverviewNCBI Gene
The protein encoded by this gene is a type I membrane protein that forms one of the two chains of a receptor for interferons alpha and beta. Binding and activation of the receptor stimulates Janus protein kinases, which in turn phosphorylate several proteins, including STAT1 and STAT2. The protein belongs to the type II cytokine receptor family and functions as an antiviral factor. [provided by RefSeq, Jul 2020]
Canonical amino-acid sequenceUniProt
557 residues, UniProt reviewed canonical sequence.
>P17181|IFNAR1
1 MMVVLLGATT LVLVAVAPWV LSAAAGGKNL KSPQKVEVDI IDDNFILRWN RSDESVGNVT
61 FSFDYQKTGM DNWIKLSGCQ NITSTKCNFS SLKLNVYEEI KLRIRAEKEN TSSWYEVDSF
121 TPFRKAQIGP PEVHLEAEDK AIVIHISPGT KDSVMWALDG LSFTYSLVIW KNSSGVEERI
181 ENIYSRHKIY KLSPETTYCL KVKAALLTSW KIGVYSPVHC IKTTVENELP PPENIEVSVQ
241 NQNYVLKWDY TYANMTFQVQ WLHAFLKRNP GNHLYKWKQI PDCENVKTTQ CVFPQNVFQK
301 GIYLLRVQAS DGNNTSFWSE EIKFDTEIQA FLLPPVFNIR SLSDSFHIYI GAPKQSGNTP
361 VIQDYPLIYE IIFWENTSNA ERKIIEKKTD VTVPNLKPLT VYCVKARAHT MDEKLNKSSV
421 FSDAVCEKTK PGNTSKIWLI VGICIALFAL PFVIYAAKVF LRCINYVFFP SLKPSSSIDE
481 YFSEQPLKNL LLSTSEEQIE KCFIIENIST IATVEETNQT DEDHKKYSSQ TSQDSGNYSN
541 EDESESKTSE ELQQDFVLocalizationUniProt · AlphaFold · HPA
Whether an antibody against IFNAR1 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
- 1
- Mean surface accessibility (rSASA)
- 0.4
- Highest tissue expression
- 32 nTPM
Expression across tissuesHPA
Tissue
- liver: 32 nTPM
- adipose tissue: 24 nTPM
- lung: 20 nTPM
- breast: 20 nTPM
- blood vessel: 19 nTPM
- salivary gland: 19 nTPM
Single-cell type
- neutrophils: 432 nCPM
- esophageal apical cells: 187 nCPM
- plasma cells: 170 nCPM
- extravillous trophoblasts: 145 nCPM
- prostatic club cells: 135 nCPM
- kupffer cells: 126 nCPM
Immune cell
- neutrophil: 17 nTPM
- basophil: 12 nTPM
- intermediate monocyte: 8.5 nTPM
- naive B-cell: 7.7 nTPM
- non-classical monocyte: 6.8 nTPM
- plasmacytoid DC: 5.9 nTPM
Brain region
- thalamus: 37 nTPM
- white matter: 34 nTPM
- spinal cord: 34 nTPM
- medulla oblongata: 34 nTPM
- pons: 34 nTPM
- hypothalamus: 32 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about IFNAR1.
Disease | AllUniProt
Conditions IFNAR1 is implicated in, by any mechanism.
- Immunodeficiency 106, susceptibility to viral infections (IMD106) MIM:619935
Disease | GeneticClinVar
23 pathogenic / likely-pathogenic of 366 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Immunodeficiency 106, susceptibility to viral infections
ReferencesPubMed · IEDB
Publications for IFNAR1 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
- Type I interferon correlates with serological and clinical manifestations of SLE.
2005 · Ann Rheum Dis · RCR 4.9 · 231 citations - MyD88 signaling in myeloid cells induces gastrointestinal tract injury and systemic inflammation after West Nile virus infection.
2026 · Cell Rep
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)
- 1.21
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.36
- DepMap mean gene effect
- 0.17
- 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
- cell surface receptor signaling pathway via JAK-STAT
- cellular response to interferon-alpha
- cellular response to interferon-beta
- cellular response to virus
- positive regulation of cellular respiration
- response to lipopolysaccharide
- response to virus
- type I interferon-mediated signaling pathway
Molecular functions
- cytokine binding
- JAK pathway signal transduction adaptor activity
- type I interferon binding
- type I interferon receptor activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of IFNAR1 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 IFNAR1 as an antibody target. Whether an autoantibody or antibody against IFNAR1 could matter depends on whether native IFNAR1 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
IFNAR1 is annotated at the cell surface, where native IFNAR1 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 IFNAR1 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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