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Data show that ten-eleven translocation 1 (TET1) suppresses tumor cell growth, migration and invasion through demethylation of CpG island in PTEN promoter by increasing 5-hmC content.
Therefore, chemical hypoxia not only causes overexpression of TET1 and TET2 but also could gradually do promoter demethylation of same genes
Overexpression of the wild-type TET1/2/3 3'UTR caused a significant increase in EZH2 (show EZH2 Proteins) expression and tumor growth, whereas the mutation in miR (show MLXIP Proteins)-26-binding sites abolished this effect.
Data show that low TET1 mRNA levels were significantly associated with worse metastases-free survival.
TET1 binds to tumor suppressor promoters and induces their re-expression through active DNA demethylation.
Loss of TET1 expression facilitates colon cancer cell migration via H3K27me3-mediated repression of E-cadherin (show CDH1 Proteins) expression.
TET1 potently inhibited canonical Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling by demethylating and upregulating two upstream antagonists of this pathway, SFRP2 (show SFRP2 Proteins) and DKK1 (show DKK1 Proteins), which was associated with inhibition of EMT (show ITK Proteins) and cancer cell metastasis.
Data suggest that the predominantly activated isoform of tet oncogene 1 protein (TET1) in cancer cells does not protect from unmethylated CpG islands (CGIs) methylation and likely mediates dynamic site-specific demethylation outside of CGIs.
MBD1 (show DPEP1 Proteins) regulates localization and activity of Tet1 in a CXXC3 (show MBD1 Proteins) domain-dependent manner.
Because the DNA hypomethylation might be a result of TET dioxygenase activity, the study examined expression of TET1-3 enzymes and the level of their product, 5-hydroxymethylcytosine (5hmC), in a panel of histologically characterized seminomas and non-seminomatous germ cell tumors. The study found highly increased expression of TET1 dioxygenase in most seminomas and strong TET1 staining in seminoma cells.
TET1 is an epigenetic determinant for regulating genes that are crucial to closure of the anterior neural tube.
TET1 regulates numerous genes defining differentiation programs in the epiblast and extraembryonic ectoderm. In epiblasts, TET1 demethylates gene promoters via hydroxymethylation and maintains telomere stability. It represses a majority of epiblast target genes independent of methylation, partly by regulation of the JMJD8 gene. Dysregulated gene expression in the absence of TET1 causes embryonic defects.
Isoform switch of TET1 regulates DNA demethylation and mouse development.
Low TET1 expression is associated with Liver Cancer.
Zfp281 interacts with Tet1, but not Tet2, and its direct transcriptional target, miR-302/367, to negatively regulate Tet2 expression to establish and maintain primed pluripotency.
Our data implicate TET enzymes ( TET1 and TET2 )in the evolutionary dynamics of TEs (show TES Proteins), both in the context of exaptation processes and of retrotransposition control. The dual role of TET action on LINE-1s may reflect the evolutionary battle between TEs (show TES Proteins) and the host
our findings reveal that TET1 forms a complex with hMOF (show KAT8 Proteins) to modulate its function and the level of H4K16Ac ultimately affect gene expression and DNA repair.
a complex relationship between ten-eleven translocation (TET) proteins and retrotransposons in mouse embryonic stem cells (ESCs (show NR2E3 Proteins)), implicating TETs as enhancers in the exaptation and function of retroelement sequences.
Tet1-mediated DNA hydroxymethylation plays a critical role in the epigenetic regulation of the Wnt (show WNT2 Proteins) pathway in intestinal stem and progenitor cells and consequently in the self-renewal of the intestinal epithelium.
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