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Dioxygenase that catalyzes the conversion of the modified genomic base 5-methylcytosine (5mC) into 5- hydroxymethylcytosine (5hmC). Additionally we are shipping TET1 Antibodies (26) and many more products for this protein.
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Noncovalent binding of ADP-ribose polymers with TET1 catalytic domain decreases TET1 hydroxylase activity while the covalent PARylation stimulates TET1 enzyme. In addition, TET1 activates PARP-1/ARTD1 (show PARP1 Proteins) independently of DNA breaks.
Expression levels of TET1 are low in renal carcinoma, particularly in high grade tumors.
our study demonstrated that DNA hypomethylation at the TET1 promoter was associated with childhood asthma in African Americans.
Identify of MLL (show MLL Proteins)-fusion/MYC (show MYC Proteins) dash, verticalmiR-26 dash, verticalTET1 signaling circuit in MLL (show MLL Proteins)-rearranged acute myeloid leukemia (show BCL11A Proteins).
The expression (mRNA and protein levels) of DNMT1 (show DNMT1 Proteins) and TET1 is increased in PFC (show CFP Proteins) of SZ and BP disorder patients.
Here, the authors reveal the methylcytosine dioxygenases TET1 and TET2 as active regulators of CTCF (show CTCF Proteins)-mediated alternative splicing through conversion of 5-methylcytosine to its oxidation derivatives.
these data suggest a dual function of GADD45a (show GADD45A Proteins) in oxidative DNA demethylation, to promote directly or indirectly TET1 activity and to enhance subsequent 5-formylcytosine/5-carboxylcytosine removal.
The downregulation of ALDOB (show ALDOB Proteins) could indicate a poor prognosis for HCC (show FAM126A Proteins) patients. In addition, ALDOB (show ALDOB Proteins) inhibits the invasive features of cell lines partly through TET1 expression.
Our study indicates that early breast cancer patients with decreased expression of TET1 mRNA had worse overall survival.
Aberrant TET1 Methylation is closely Associated with CpG Island Methylator Phenotype in Colorectal Cancer
Reprogramming of spermatogonial stem cells from Tet1 and Tet2 double knockout mice however lacked demethylation of H19 (show NCKAP1 Proteins) imprinting control regions.
The critical roles of TET1/2 individually.
These results uncover the hypermethylation of DNA methylation canyons as the genomic key feature of Tet1/Tet2 double-knockout mouse embryonic fibroblasts.
Lin28A (show LIN28A Proteins) binds active promoters and recruits Tet1 to regulate gene expression via epigenetic DNA modifications.
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
findings demonstrate that DAZL (show DAZL Proteins) associates with mRNA of Tet1, a catalyst of 5-hydroxylation of methyl-cytosine, and enhances Tet1 mRNA translation; DAZL (show DAZL Proteins) enhances TET1-mediated cytosine hydroxymethylation in embryonic stem cells that are actively reprogramming to a pluripotent ground state
The miR (show MLXIP Proteins)-29b/Tet1 regulatory axis promotes the mesendoderm lineage formation by inducing the Nodal signaling pathway and repressing the key target of the active demethylation pathway, thymine DNA glycosylase (show TDG Proteins).
Both TET1 and TET2 are required for the repression of embryonic stem cells differentiation by PRDM14 (show PRDM14 Proteins).
This study expands the knowledge about Tet1 involvement in stemness circuits in embryonic stem cells and provides evidence for a transcriptional relationship between Tet1 and Polycomb (show CBX2 Proteins) repressive complex 2 in adult proliferating cells.
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 dioxygenase was present in the very first embryo stages, in contrast to TET1 and AICDA (show AICDA Proteins).
Dioxygenase that catalyzes the conversion of the modified genomic base 5-methylcytosine (5mC) into 5- hydroxymethylcytosine (5hmC). Might initiate a process leading to cytosine demethylation through deamination into 5- hydroxymethyluracil (5hmU) and subsequent replacement by unmethylated cytosine by the base excision repair system. Methylation at the C5 position of cytosine bases is an epigenetic modification of the mammalian genome which plays an important role in transcriptional regulation. Preferentially binds to CpG-rich sequences at promoters of both transcriptionally active and polycomb-repressed genes. By controlling the levels of 5mC and 5hmC at gene promoters, it may regulate the gene expression silencing induced by cytosine methylation. May have a dual function by also repressing the expression of a subset of genes through recruitment of transcriptional repressors to promoters. Involved in the balance between pluripotency and lineage commitment of cells it plays a role in embryonic stem cells maintenance and inner cell mass cell specification.
CXXC finger 6
, CXXC zinc finger 6
, CXXC-type zinc finger protein 6
, leukemia-associated protein with a CXXC domain
, methylcytosine dioxygenase TET1
, ten-eleven translocation 1 gene protein
, ten-eleven translocation-1
, tet oncogene 1
, ten-eleven translocation 1 gene protein homolog
, tet methylcytosine dioxygenase 1