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Members of the ten-eleven translocation (TET) gene family, including TET3, play a role in the DNA methylation process (Langemeijer et al., 2009 [PubMed 19923888]).[supplied by OMIM, Nov 2010].. Additionally we are shipping TET3 Antibodies (86) and and many more products for this protein.
TET3 expression inhibits glioblastoma tumorigenesis and self-renewal in glioblastoma stem cells.
levels of TET3 and TDG (show TDG ELISA Kits) mRNAs were independent prognostic factors for early breast cancer patients who received anthracycline chemotherapy
Hypoxia deregulates TET3. TET1/3 levels were associated with tumor hypoxia, tumor malignancy, and poor prognosis in breast cancer patients. Coordinate functions of TET1 and TET3 were needed to activate TNFalpha (show TNF ELISA Kits)-p38-MAPK (show MAPK14 ELISA Kits) signaling in hypoxia.
In hepatic stellate cells, cell proliferation rise significantly and cell apoptosis reduce obviously after knockdown of TET3.
GABRA3 (show GABRA3 ELISA Kits) also carries a microRNA (miR (show MLXIP ELISA Kits)-767) with predicted target sites in TET1 and TET3, two members of the ten-eleven-translocation family of tumor suppressor genes, involved in the conversion of 5-methylcytosines to 5-hydroxymethylcytosines in DNA.
TET1, TET2 (show TET2 ELISA Kits), and TET3 are highly phosphorylated.
TET1 depletion yields widespread reduction of 5hmC, while depletion of TET2 and TET3 reduces 5hmC at a subset of TET1 targets suggesting functional co-dependence.
OGT (show OGT ELISA Kits) catalyzes the O-GlcNAcylation of TET3, promotes TET3 nuclear export, and, consequently, inhibits the formation of 5-hydroxymethylcytosine catalyzed by TET3.
TET3 enhanced its localization to chromatin through the stabilization of OGT (show OGT ELISA Kits) protein.
MiR (show MLXIP ELISA Kits)-29a mimics decrease the levels of Tet1, Tet2 (show TET2 ELISA Kits), and Tet3; miR (show MLXIP ELISA Kits)-29a inhibition increases all three Tets in human dermal fibroblasts.
The CXXC domain of Tet3 has the capacity to bind to unmethylated and carboxylated cytosines at CpG sequences and a very restricted genomic localization pattern with a preference for transcription start sites.
Genetic ablation of TET3 in oocytes had no significant effect on oocyte development.
the stability of Foxp3 (show FOXP3 ELISA Kits) expression is markedly compromised in T reg (show KCNH2 ELISA Kits) cells from Tet2 (show TET2 ELISA Kits)/Tet3 double-deficient mice.
The DNA demethylation marks are dynamically regulated in both in vivo and in vitro aging conditions, which are associated with Tet3 over-expression and Tdg (show TDG ELISA Kits) repression.
Knockdown of Tet1 and Tet3 by RNAi in ex vivo cerebellar slice cultures inhibits dendritic arborization of developing cerebellar granule cells, a critical step in circuit formation
This paper demonstrates a Tet3-dependent mechanism underlying the dexamethasone-induced epigenetic reprogramming leading to heritable alterations of a fundamental player in cortical development.
We propose a mechanism for transcriptional activation in neurons that involves REST-guided targeting of TET3 to the DNA for directed 5hmC generation and NSD3 (show WHSC1L1 ELISA Kits)-mediated H3K36 trimethylation
results not only reveal a link between miRNAs, TET, and DNA demethylation but also demonstrate critical roles for miR (show MLXIP ELISA Kits)-15b and TET3 in maintaining the NPC (show NPC1 ELISA Kits) pool during early neocortical development.
Embryos lacking Tet1 and Tet3 (Tet1/3 DKO) displayed a strong loss of 5-hydroxymethylcytosine (5hmC) and a concurrent increase in 5-methylcytosine (5mC) at the eight-cell stage.
Tet3 is important for neural progenitor cell maintenance and terminal differentiation of neurons.
Members of the ten-eleven translocation (TET) gene family, including TET3, play a role in the DNA methylation process (Langemeijer et al., 2009
probable methylcytosine dioxygenase TET3
, tet oncogene family member 3
, methylcytosine dioxygenase TET3