SCUBA

CXCR3 — C-X-C motif chemokine receptor 3

CXCR3 belongs to a gene co-expression module in 2 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

CXCR3's module in each cell type

Cell typeModuleShares the module with
CD8⁺ T cellsEffector-Memory CD8
T cell maturation
CD27, CD44, CMC1, CST7, DUSP2, EOMES, F2R, HLA-E +8 moreView in SCUBA
Gamma-delta T cellsDeath Receptor Apoptosis
Stress
FHL3, GABARAPL2, LDLRAP1, LY6E, PDGFB, PLSCR3, SGSM3, SHISAL2A +4 more

About the gene

SynonymsCD183, CKR-L2, CMKAR3, GPR9, IP10-R, MigR
ChromosomeX: 71615916-71618511
Predicted locationMembrane
Essential geneNo
Protein classCD markers, G-protein coupled receptors, Predicted membrane proteins
Molecular functionG-protein coupled receptor, Receptor, Transducer
Biological processAngiogenesis, Apoptosis, Chemotaxis

Function

Receptor for the C-X-C chemokine CXCL9, CXCL10 and CXCL11 and mediates the proliferation, survival and angiogenic activity of human mesangial cells (HMC) through a heterotrimeric G- protein signaling pathway. Binds to CCL21. Probably promotes cell chemotaxis response. Upon activation by PF4, induces activated T-lymphocytes migration mediated via downstream Ras/extracellular signal-regulated kinase (ERK) signaling. Receptor for the C-X-C chemokine CXCL4 and also mediates the inhibitory activities of CXCL9, CXCL10 and CXCL11 on the proliferation, survival and angiogenic activity of human microvascular endothelial cells (HMVEC) through a cAMP-mediated signaling pathway. Does not promote cell chemotaxis respons. Interaction with CXCL4 or CXCL10 leads to activation of the p38MAPK pathway and contributes to inhibition of angiogenesis. Overexpression in renal cancer cells down-regulates expression of the anti-apoptotic protein HMOX1 and promotes apoptosis. Mediates the activity of CXCL11

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.