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interferon α/β receptor 1

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Immunopharmacology Ligand target has curated data in GtoImmuPdb

Target id: 1723

Nomenclature: interferon α/β receptor 1

Family: Interferon receptor family

Quaternary Structure: Complexes
Interferon-α/β receptor
Gene and Protein Information Click here for help
Species TM AA Chromosomal Location Gene Symbol Gene Name Reference
Human 1 557 21q22.11 IFNAR1 interferon alpha and beta receptor subunit 1
Mouse 1 590 16 52.98 cM Ifnar1 interferon (alpha and beta) receptor 1
Rat - - Ifnar1 interferon alpha and beta receptor subunit 1
Previous and Unofficial Names Click here for help
IFRC | interferon (alpha and beta) receptor 1 | interferon (alpha, beta and omega) receptor 1 | Ifar | IFN-alpha/betaR
Database Links Click here for help
Alphafold
CATH/Gene3D
ChEMBL Target
DrugBank Target
Ensembl Gene
Entrez Gene
Human Protein Atlas
KEGG Gene
OMIM
Pharos
UniProtKB
Wikipedia
Natural/Endogenous Ligands Click here for help
IFN-β {Sp: Human}

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Agonists
Key to terms and symbols Click column headers to sort
Ligand Sp. Action Value Parameter Reference
IFN-β {Sp: Human} Peptide Click here for species-specific activity table Ligand is endogenous in the given species Immunopharmacology Ligand Hs Agonist 7.8 pKd 5
pKd 7.8 (Kd 1.58x10-8 M) [5]
Description: Measured using a surface plasmon resonance (SPR) assay, and recombinant hIFNAR1-extracellular domain (ECD) expressed in insect cells.
peginterferon alfa-2b Peptide Approved drug Primary target of this compound Click here for species-specific activity table Immunopharmacology Ligand Hs Agonist - - 4
[4]
Antibodies
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Antibody Sp. Action Value Parameter Reference
anifrolumab Peptide Approved drug Primary target of this compound Immunopharmacology Ligand Hs Binding >10.0 pKd 1
pKd >10.0 (Kd <1x10-10 M) [1]
Immunopharmacology Comments
IFNAR1 is a subunit of the functional receptor for type I interferons (NOT interferon γ). Type I interferons (IFN) exhibit an established anti-viral action. However, type I IFN signalling also appears to play a role in impaired resistance to a range of other pathogens (e.g. bacterial infection) [2-3]. A rare mutation in IFNAR1, identified in the Chinese population, that impairs type I IFN signalling, is associated with increased resistance to tuberculosis infection and reduced TB symptoms [5].
Immuno Process Associations
Immuno Process:  Inflammation
Immuno Process:  Cytokine production & signalling
Immuno Process:  Cellular signalling
Immuno Process:  T cell (activation)
Biologically Significant Variants Click here for help
Type:  Insertion/deletion
Species:  Human
Description:  An in-frame deletion of a nucleotide codon that corresponds to a proline deletion in IFNAR1, reduces type I interferon binding affinity and increases resistance to tuberculosis infection and reduces TB pathology.
Amino acid change:  Pro335del
Nucleotide change:  TCCdel
SNP accession: 
References:  5

References

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1. Cardarelli JM, Witte A, Srinivasan M. (2010) Interferon alpha receptor I antibodies and their use. Patent number: US7662381. Assignee: Medarex, Inc.. Priority date: 21/06/2004. Publication date: 16/02/2010.

2. Carrero JA. (2013) Confounding roles for type I interferons during bacterial and viral pathogenesis. Int Immunol, 25 (12): 663-9. [PMID:24158954]

3. Ng CT, Mendoza JL, Garcia KC, Oldstone MB. (2016) Alpha and Beta Type 1 Interferon Signaling: Passage for Diverse Biologic Outcomes. Cell, 164 (3): 349-52. [PMID:26824652]

4. Ward AC, Touw I, Yoshimura A. (2000) The Jak-Stat pathway in normal and perturbed hematopoiesis. Blood, 95 (1): 19-29. [PMID:10607680]

5. Zhang G, deWeerd NA, Stifter SA, Liu L, Zhou B, Wang W, Zhou Y, Ying B, Hu X, Matthews AY et al.. (2018) A proline deletion in IFNAR1 impairs IFN-signaling and underlies increased resistance to tuberculosis in humans. Nat Commun, 9 (1): 85. [PMID:29311663]

How to cite this page

Interferon receptor family: interferon α/β receptor 1. Last modified on 18/01/2018. Accessed on 19/04/2024. IUPHAR/BPS Guide to PHARMACOLOGY, https://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=1723.