SCUBA

TCIM — Transcriptional and immune response regulator

TCIM 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.

TCIM's module in each cell type

Cell typeModuleShares the module with
EndothelialGlucocorticoid Response
Endothelial cell development
APOLD1, DENND3, DPYSL2, JAM3, KLF11, KLF9, MFSD6, NDRG1 +8 moreView in SCUBA
FibroblastsNF-κB Stress Response
Inflammatory
EGR3, NAMPT, NCOA7, NFIL3, PHLDA1, PHLDA2, SAT1, SLC20A1 +3 moreView in SCUBA
Goblet cellsActin Cytoskeletal Remodeling
Cytoskeletal
ACTN4, ACTR3, BHLHE40, CAP1, FHL2, KCNK1, LRP10, SDCBP +3 moreView in SCUBA
Smooth muscle cellsTelocyte/Fibroblast Contamination
Cell contamination
ABI3BP, ADH1B, ASB2, BCHE, BMP4, C5orf66-AS1, CDCA7L, FENDRR +5 moreView in SCUBA

About the gene

SynonymsC8orf4, hTC-1, TC-1, TC1
Chromosome8: 40153482-40155310
Predicted locationIntracellular
Essential geneNo
Protein classPredicted intracellular proteins
Biological processApoptosis

Function

Seems to be involved in the regulation of cell growth an differentiation, may play different and opposite roles depending on the tissue or cell type. May enhance the WNT-CTNNB1 pathway by relieving antagonistic activity of CBY1. Enhances the proliferation of follicular dendritic cells. Plays a role in the mitogen-activated MAPK2/3 signaling pathway, positively regulates G1-to-S-phase transition of the cell cycle. In endothelial cells, enhances key inflammatory mediators and inflammatory response through the modulation of NF-kappaB transcriptional regulatory activity. Involved in the regulation of heat shock response, seems to play a positive feedback with HSF1 to modulate heat-shock downstream gene expression. Plays a role in the regulation of hematopoiesis even if the mechanisms are unknown (By similarity). In cancers such as thyroid or lung cancer, it has been described as promoter of cell proliferation, G1-to-S-phase transition and inhibitor of apoptosis. However, it negatively regulates self-renewal of liver cancer cells via suppresion of NOTCH2 signaling.

Human Protein Atlas · Open Targets · UniProt

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