TIGIT — T cell immunoreceptor with Ig and ITIM domains
TIGIT belongs to a gene co-expression module in 4 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.
TIGIT's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| CD4⁺ T cells | Regulatory T cell Immune regulation | ACTA2, APOLD1, ATP13A3, CARD16, CD27, CD79B, DNAH8, FAM184A +7 more | View in SCUBA |
| CD8⁺ T cells | Cytotoxic Exhausted CD8 Exhaustion | CCL3, CD2BP2, CLEC2D, CTSD, DUSP4, GZMB, NDFIP2, PHLDA1 +2 more | View in SCUBA |
| Gamma-delta T cells | T Cell Exhaustion Exhaustion | AKAP5, AOAH, CCDC141, CD8A, CD8B, CDYL, CRTAM, CYSTM1 +20 more | |
| Natural Killer cells | NK Cytotoxic Activation Cytotoxicity | CALR, CDK6, FASLG, P4HB, PDIA3, PPIB, SLAMF7, STARD3NL +1 more | View in SCUBA |
About the gene
| Synonyms | DKFZp667A205, FLJ39873, VSIG9, VSTM3 |
|---|---|
| Chromosome | 3: 114276913-114310288 |
| Predicted location | Membrane |
| Essential gene | No |
| Protein class | Predicted membrane proteins |
Function
Inhibitory receptor that plays a role in the modulation of immune responses. Suppresses T-cell activation by promoting the generation of mature immunoregulatory dendritic cells. Upon binding to its ligands PVR/CD155 or NECTIN2/CD112, which are expressed on antigen-presenting cells, sends inhibitory signals to the T-cell or NK cell. Mechanistically, interaction with ligand leads to phosphorylation of the cytoplasmic tail by Src family tyrosine kinases such as FYN or LCK, allowing subsequent binding to adapter GRB2 and SHIP1/INPP5D. In turn, inhibits PI3K and MAPK signaling cascades. In addition, associates with beta-arrestin-2/ARRB2 to recruit SHIP1/INPP5D that suppresses autoubiquitination of TRAF6 and subsequently inhibits NF- kappa-B signaling pathway. Also acts as a receptor for NECTIN4 to inhibit NK cell cytotoxicity.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.