Description: Homo sapiens interleukin 23 receptor (IL23R), mRNA. RefSeq Summary (NM_144701): 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. [provided by RefSeq, Jul 2008]. Transcript (Including UTRs) Position: hg19 chr1:67,635,025-67,725,650 Size: 90,626 Total Exon Count: 8 Strand: + Coding Region Position: hg19 chr1:67,672,703-67,724,811 Size: 52,109 Coding Exon Count: 6
ID:IL23R_HUMAN DESCRIPTION: RecName: Full=Interleukin-23 receptor; Short=IL-23 receptor; Short=IL-23R; Flags: Precursor; FUNCTION: Associates with IL12RB1 to form the interleukin-23 receptor. Binds IL23 and mediates T-cells, NK cells and possibly certain macrophage/myeloid cells stimulation probably through activation of the Jak-Stat signaling cascade. IL23 functions in innate and adaptive immunity and may participate in acute response to infection in peripheral tissues. IL23 may be responsible for autoimmune inflammatory diseases and be important for tumorigenesis. SUBUNIT: Heterodimer with IL12RB1. In presence of IL23, the heterodimer forms the IL23 receptor. Interacts with JAK2 and in presence of IL23 with STAT3. SUBCELLULAR LOCATION: Cell membrane; Single-pass type I membrane protein. TISSUE SPECIFICITY: Expressed by monocytes, Th1, Th0, NK and dendritic cells. Isoform 1 is specifically expressed in NK cells. PTM: Phosphorylated in response to IL23. DISEASE: Genetic variations in IL23R are associated with inflammatory bowel disease type 17 (IBD17) [MIM:612261]. IBD17 is a chronic, relapsing inflammation of the gastrointestinal tract with a complex etiology. It is subdivided into Crohn disease and ulcerative colitis phenotypes. Crohn disease may affect any part of the gastrointestinal tract from the mouth to the anus, but most frequently it involves the terminal ileum and colon. Bowel inflammation is transmural and discontinuous; it may contain granulomas or be associated with intestinal or perianal fistulas. In contrast, in ulcerative colitis, the inflammation is continuous and limited to rectal and colonic mucosal layers; fistulas and granulomas are not observed. Both diseases include extraintestinal inflammation of the skin, eyes, or joints. DISEASE: Genetic variations in IL23R are a cause of susceptibility to psoriasis type 7 (PSORS7) [MIM:605606]. Psoriasis is a common, chronic inflammatory disease of the skin with multifactorial etiology. It is characterized by red, scaly plaques usually found on the scalp, elbows and knees. These lesions are caused by abnormal keratinocyte proliferation and infiltration of inflammatory cells into the dermis and epidermis. SIMILARITY: Belongs to the type I cytokine receptor family. Type 2 subfamily. SIMILARITY: Contains 2 fibronectin type-III domains. SEQUENCE CAUTION: Sequence=AAH16829.1; Type=Erroneous initiation; Note=Translation N-terminally shortened; Sequence=CAH70408.1; Type=Erroneous initiation; Note=Translation N-terminally shortened; Sequence=CAI22679.1; Type=Erroneous initiation; Note=Translation N-terminally shortened;
Bernd Gruhn , et al. Biology of blood and marrow transplantation 2009 15(12):1571-7, Polymorphism of interleukin-23 receptor gene but not of NOD2/CARD15 is associated with graft-versus-host disease after hematopoietic stem cell transplantation in children., Biology of blood and marrow transplantation 2009 15(12):1571-7.
[PubMed 19896081]
Behcet Syndrome Elaine F Remmers et al. Nature genetics 2010, , Nature genetics.
[PubMed 20622878]
Behcet Syndrome Elaine F Remmers et al. Nature genetics 2010, , Nature genetics.
[PubMed 20622878]
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on Q5VWK5
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.
Biological Process: GO:0001916 positive regulation of T cell mediated cytotoxicity GO:0002230 positive regulation of defense response to virus by host GO:0002376 immune system process GO:0002827 positive regulation of T-helper 1 type immune response GO:0006954 inflammatory response GO:0010536 positive regulation of activation of Janus kinase activity GO:0019221 cytokine-mediated signaling pathway GO:0032496 response to lipopolysaccharide GO:0032693 negative regulation of interleukin-10 production GO:0032725 positive regulation of granulocyte macrophage colony-stimulating factor production GO:0032729 positive regulation of interferon-gamma production GO:0032735 positive regulation of interleukin-12 production GO:0032740 positive regulation of interleukin-17 production GO:0032819 positive regulation of natural killer cell proliferation GO:0034341 response to interferon-gamma GO:0038155 interleukin-23-mediated signaling pathway GO:0042102 positive regulation of T cell proliferation GO:0042104 positive regulation of activated T cell proliferation GO:0042509 regulation of tyrosine phosphorylation of STAT protein GO:0042531 positive regulation of tyrosine phosphorylation of STAT protein GO:0043382 positive regulation of memory T cell differentiation GO:0045087 innate immune response GO:0045672 positive regulation of osteoclast differentiation GO:0050829 defense response to Gram-negative bacterium GO:0051135 positive regulation of NK T cell activation GO:2000318 positive regulation of T-helper 17 type immune response GO:2000330 positive regulation of T-helper 17 cell lineage commitment
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