Cancer Protein Description

This report provides a detailed description of a selected cancer protein with information collected from various sources, including UniProt, the Wellcome Trust Sanger Institute’s Catalogue of Somatic Mutations in Cancer (COSMIC), and the Atlas of Genetics and Cytogenetics in Oncology and Haematology.


Protein Name: CXCR3
Gene Name: CXCR3
Protein Full Name: C-X-C chemokine receptor type 3
Alias: CD183; CD183 antigen; Chemokine (C-X-C motif) receptor 3; CKR-L2; CMKAR3; CXC-R3; CXCR-3; G protein-coupled receptor 9; GPR9; Interferon-inducible protein 10 receptor; IP10; IP10 receptor; IP-10 receptor; IP10-R; Mig receptor; MigR; Mig-R
Mass (Da): 40660
Number AA: 368
UniProt ID: P49682
Locus ID: 2833
COSMIC ID: CXCR3
Gene location on chromosome: Xq13.1
Cancer protein type: MIXED (Isoform A = OP; Isoform B = TSP)
Effect of cancer mutation on protein: UNCLEAR
Effect of active protein on cancer: MIXED
Number of cancer specimens: 20149
Percent of cancer specimens with mutations: 0.29
Mutations observed as inherited: NA
Found in amplified chromosomal regions in human cancers: NA
Deregulated in translocations: NA
Deregulated by viral insertion: NA
Transduced into viral genome: NA
Gene undergoes hypermethylation: NA
Normal role description: CXCR3 is a G protein coupled receptor that mediates the proliferation of mesangial cells in the kidneys via binding of ligands including CXCL9/10/11. A second isoform, CXCR3B, is also a receptor for CXCL4 and plays a role in the inhibition of growth of microvascular endothelial cells and thus may play a role in regulating angiogenesis. Other functions include leukocyte trafficking via integrin activation, cytoskeletal changes and chemotactic migration. CXCR3 has been associated with the migration of malignant B cells from chronic lymphoproliferative disorders such as CLL. Overexpression of CXCR3A (isoform A) increased endothelial cell survival, but overexpression of CXCR3B increased apoptotic pathways. In a murine model with B16F10 melanoma cells, CXCR3 downregulation decreased metastatic activities to lymph nodes. Similar effects have been seen with breast cancer cells and colon cancer cells. It has been noted that RAS activation in breast cancer cells downregulates CXCR3B isoform to promote tumour cell proliferation, presumeably by decreasing CXCR3B-mediated apoptosis.


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