SCUBA

TET2 — Tet methylcytosine dioxygenase 2

TET2 belongs to a gene co-expression module in 3 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.

TET2's module in each cell type

Cell typeModuleShares the module with
CD19⁺ B cellsAtypical memory B cell
B cell maturation
FCRL5, FGR, HCK, HEXA, HMOX1, ITGAX, LRRK2, MED13L +5 moreView in SCUBA
CD4⁺ T cellsEpigenetic regulation
DNA/chromatin regulation
AFF4, ARID1B, CTSA, DGKH, FUBP1, JARID2, PDCD6, SYNCRIP +6 moreView in SCUBA
MacrophagesEpigenetic Remodeling
Housekeeping
AFF4, AGO3, AKAP13, ARID4B, ASH1L, CYTH1, ELF1, EPC1 +16 moreView in SCUBA

About the gene

SynonymsFLJ20032, KIAA1546
Chromosome4: 105145875-105279816
Predicted locationIntracellular
Essential geneNo
Protein classCancer-related genes, Disease related genes, Enzymes, Human disease related genes, Potential drug targets, Predicted intracellular proteins
Molecular functionChromatin regulator, Dioxygenase, DNA-binding, Oxidoreductase
Biological processCell cycle

Function

Dioxygenase that catalyzes the conversion of the modified genomic base 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC) and plays a key role in active DNA demethylation. Has a preference for 5-hydroxymethylcytosine in CpG motifs. Also mediates subsequent conversion of 5hmC into 5-formylcytosine (5fC), and conversion of 5fC to 5-carboxylcytosine (5caC). Conversion of 5mC into 5hmC, 5fC and 5caC probably constitutes the first step in cytosine demethylation. Methylation at the C5 position of cytosine bases is an epigenetic modification of the mammalian genome which plays an important role in transcriptional regulation. In addition to its role in DNA demethylation, also involved in the recruitment of the O-GlcNAc transferase OGT to CpG-rich transcription start sites of active genes, thereby promoting histone H2B GlcNAcylation by OGT.

Human Protein Atlas · Open Targets · UniProt

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