SCUBA

IDO1 — Indoleamine 2,3-dioxygenase 1

IDO1 belongs to a gene co-expression module in 5 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.

IDO1's module in each cell type

Cell typeModuleShares the module with
EndothelialIFN-gamma Response
Inflammation
APOL2, APOL6, BATF2, CARD16, CASP1, CD40, CXCL10, CXCL11 +18 moreView in SCUBA
FibroblastsIFN-γ MHC-II Response
Inflammatory
CALHM6, CD74, CXCL11, CXCL9, GBP4, HLA-DPA1, HLA-DPB1, HLA-DQA1 +3 moreView in SCUBA
Glial cellsIFN-gamma Effector Program
Inflammation
APOL1, APOL2, GBP1, IFI44L, IL18BP, IL32, LAP3, ODF3B +5 moreView in SCUBA
MacrophagesIFN-gamma Response
Inflammatory
ANKRD22, APOL2, ATF5, ATP13A1, CD274, CD300LF, CD40, CD48 +21 moreView in SCUBA
MonocytesTolerogenic Monocyte Activation
Inflammatory
CCR5, CD40, CD80, GGT5, IL4I1, MANF, PLA2G7, SLAMF7 +1 moreView in SCUBA

About the gene

SynonymsIDO, INDO
Chromosome8: 39902275-39928790
Predicted locationIntracellular
Essential geneNo
Protein classCancer-related genes, Enzymes, Metabolic proteins, Predicted intracellular proteins
Molecular functionDioxygenase, Oxidoreductase
Biological processImmunity, Tryptophan catabolism

Function

Catalyzes the first and rate limiting step of the catabolism of the essential amino acid tryptophan along the kynurenine pathway. Involved in the peripheral immune tolerance, contributing to maintain homeostasis by preventing autoimmunity or immunopathology that would result from uncontrolled and overreacting immune responses. Tryptophan shortage inhibits T lymphocytes division and accumulation of tryptophan catabolites induces T-cell apoptosis and differentiation of regulatory T-cells. Acts as a suppressor of anti-tumor immunity. Limits the growth of intracellular pathogens by depriving tryptophan. Protects the fetus from maternal immune rejection.

Human Protein Atlas · Open Targets · UniProt

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