Interleukin-23 receptor

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Interleukin 23 receptor
Symbol IL23R
External IDs OMIM607562 MGI2181693 HomoloGene16930 GeneCards: IL23R Gene
Species Human Mouse
Entrez 149233 209590
Ensembl ENSG00000162594 ENSMUSG00000049093
UniProt Q5VWK5 Q8K4B4
RefSeq (mRNA) NM_144701 NM_144548
RefSeq (protein) NP_653302 NP_653131
Location (UCSC) Chr 1:
67.17 – 67.26 Mb
Chr 6:
67.42 – 67.49 Mb
PubMed search [1] [2]

Interleukin 23 receptor is a type I cytokine receptor. IL23R is its human gene.[1]

The protein encoded by this gene is a subunit of the receptor for IL23A/IL23. This protein pairs with the receptor molecule IL12RB1/IL12Rbeta1, and both are required for IL23A signaling. This protein associates constitutively with Janus kinase 2 (JAK2), and also binds to transcription activator STAT3 in a ligand-dependent manner.[1]

Clinical significance[edit]

Three variants in the IL23R gene have been shown to protect against Crohn's disease and ulcerative colitis.[2][3][4]

Model organisms[edit]

Model organisms have been used in the study of IL23R function. A conditional knockout mouse line called Il23rtm2a(EUCOMM)Wtsi was generated at the Wellcome Trust Sanger Institute.[5] Male and female animals underwent a standardized phenotypic screen[6] to determine the effects of deletion.[7][8][9][10] Additional screens performed: - In-depth immunological phenotyping[11]


  1. ^ a b "Entrez Gene: IL23R interleukin 23 receptor". 
  2. ^ Duerr, Richard; et al. (2006). "A genome-wide association study identifies IL23R as an inflammatory bowel disease gene.". Science 314 (5804): 1461-1463. PMID 17068223. 
  3. ^ Rivas, Manuel; et al. (2011). "Deep resequencing of GWAS loci identifies independent rare variants associated with inflammatory bowel disease". Nature Genetics 43 (11): 1066–1073. 
  4. ^ Momozawa, Yukihide; et al. (2011). "Resequencing of positional candidates identifies low frequency IL23R coding variants protecting against inflammatory bowel disease.". Nature Genetics 43 (1): 43–47. 
  5. ^ Gerdin AK (2010). "The Sanger Mouse Genetics Programme: high throughput characterisation of knockout mice". Acta Opthalmologica 88: 925-7.doi:10.1111/j.1755-3768.2010.4142.x: Wiley. 
  6. ^ a b "International Mouse Phenotyping Consortium". 
  7. ^ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (Jun 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750. 
  8. ^ Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718. 
  9. ^ Collins FS, Rossant J, Wurst W (Jan 2007). "A mouse for all reasons". Cell 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247. 
  10. ^ White JK, Gerdin AK, Karp NA, Ryder E, Buljan M, Bussell JN, Salisbury J, Clare S, Ingham NJ, Podrini C, Houghton R, Estabel J, Bottomley JR, Melvin DG, Sunter D, Adams NC, Sanger Institute Mouse Genetics Project, Tannahill D, Logan DW, Macarthur DG, Flint J, Mahajan VB, Tsang SH, Smyth I, Watt FM, Skarnes WC, Dougan G, Adams DJ, Ramirez-Solis R, Bradley A, Steel KP (2013). "Genome-wide generation and systematic phenotyping of knockout mice reveals new roles for many genes". Cell 154 (2): 452–64. doi:10.1016/j.cell.2013.06.022. PMID 23870131. 
  11. ^ a b "Infection and Immunity Immunophenotyping (3i) Consortium". 

Further reading[edit]