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anti-Human TET1 Antibodies:
anti-Mouse (Murine) TET1 Antibodies:
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Human Polyclonal TET1 Primary Antibody for ChIPSeq, ChIP - ABIN2668522
Feng, Wang, Li, Zeng, Kuang, Li, Yue: TET1-mediated different transcriptional regulation in prostate cancer. in International journal of clinical and experimental medicine 2015
Show all 2 Pubmed References
Mouse (Murine) Monoclonal TET1 Primary Antibody for ICC, IF - ABIN5563987
Bauer, Göbel, Nagaraj, Colantuoni, Wang, Müller, Kremmer, Rottach, Leonhardt: Phosphorylation of TET proteins is regulated via O-GlcNAcylation by the O-linked N-acetylglucosamine transferase (OGT). in The Journal of biological chemistry 2015
Show all 2 Pubmed References
Human Polyclonal TET1 Primary Antibody for ICC, IF - ABIN4358581
Zhao, Zhang, Xia, Zhou, Cao: Promoter demethylation of nuclear factor-erythroid 2-related factor 2 gene in drug-resistant colon cancer cells. in Oncology letters 2015
Human Monoclonal TET1 Primary Antibody for ChIP, ICC - ABIN4247103
Agrawal, Das, Táborská, Gurský, Džubák, Hajdúch: Differential Regulation of Methylation-Regulating Enzymes by Senescent Stromal Cells Drives Colorectal Cancer Cell Response to DNA-Demethylating Epi-Drugs. in Stem cells international 2018
TET1 expression was downregulated in nasopharyngeal carcinoma (NPC) tissues. Demethylation of TET1 in NPC cell lines cells restored its expression with downregulated methylation, implying that TET1 was silenced by promoter hypermethylation. Data provide evidence that TET1 exerts its anti-tumor functions in NPC cells by suppressing Wnt/beta-catenin signaling via demethylation of Wnt antagonists (DACT2 and SFRP2).
It has been demonstrated that the activities of Tet enzymes display distinct patterns of oxygen dependency, and that Tet1 activity, specifically, is subject to differential regulation within a range of O2 which is physiologically relevant in embryogenesis.
TET1 is one of the targets of miR-365a-3p. miR-365a-3p regulates the biological behavior of laryngeal cancer by down-regulating TET1.
Low TET1 expression is associated with gastric cancer.
Mono-ADP-ribosylation of H3R117 upregulated methylation of TFPI2 by impact TET1.
a single transient transfection of Ten-eleven translocation 1 catalytic domain on hepatocellular carcinoma
Genomic profiling in embryonic stem cells identifies thousands of R-loop-dependent TET1 binding sites at CGIs.
TET1 may affect the development and progression of gliomas by influencing 5mC and 5hmC levels of functional genes such as some proteins-binding and nucleic acid-binding gene, and some signaling pathways including Hippo and TGF-[beta] signaling pathways. In addition, it can also affect the level of autophagy-related gene ATG13 and DRAM1 in glioma and U251 cell, thereby influencing the occurrence and development of gliomas.
Aberrant methylation of TP53 promoter as a result of reduced TET1 and 5-hydroxymethylcytosine may be involved in the acquisition of aggressive behavior in gastric adenocarcinoma with enteroblastic differentiation.
abnormal expression in eutopic endometrium from infertile women with endometriosis
TET1 recruits SIN3A and EZH2 to osteogenic genes.
Hypoxia-induced TET1 expression facilitates trophoblast cell migration and invasion through the HIF1alpha signaling pathway.
Analyzed involvement of 5-hydroxymethylcytosine (5hmC), tet methylcytosine dioxygenase 1 (TET1) and tet methylcytosine dioxygenase 2 (TET2) in small intestinal neuroendocrine tumors.
The expression of TET1, TET2, and TET3 was lower in the villi in early pregnancy loss group than in normal pregnancy group
Our study demonstrates the existence of a TET1/DUOX2/ROS/EMT axis that could play a role in colon cancer chemo-resistance and the aggressiveness of this cancer.
this study illustrates the involvement of TET1 in the different arms of the DNA damage response (DDR) and suggests its loss results in the continued survival of cells with genomic instability
Data show that knockdown of STAT transcription factors STAT3 and/or STAT5 reduces DNA methylcytosine dioxygenase Ten-eleven translocation 1 (TET1) level.
data demonstrated that miR4284 could promote tumor cell growth, migration and invasion by directly targeting TET1 in gastric cancer, which may provide a potential therapeutic target for gastric cancer treatment.
Low TET1 expression is associated with colorectal cancer.
These data indicate that AA has the potential to modify TET function in lymphoma and enhance chemosensitivity. In addition, the AA deficiency seen in some patients may further impair TET function and contribute to resistance. Clinical trials testing intravenous AA with chemotherapy are warranted.
Sin3a interacted with Tet1 to facilitate the transcription of a set of their co-target genes in embryonic stem cells
Pluripotency transcription factors and Tet1/2 maintain Brd4-independent stem cell identity in mouse embryonic stem cells.
we show that disrupting the TET1-OGT interaction in mouse embryonic stem cells changes the abundance of TET2 and 5-methylcytosine, which is accompanied by alterations in gene expression.
Results indicate that tet oncogene 1 protein (Tet1) and tet oncogene 2 protein (Tet2) play a critical role in maintaining bone marrow MSCs (BMMSCs) and bone homeostasis through demethylation of P2X7 purinoceptor (P2rX7) to control exosome and miRNA release.
DNMT3A and TET1 regulate the epigenome and gene expression at specific targets via their functional interplay.
Tet1 overexpression affected adult neurogenesis with oligodendrocyte differentiation in the hippocampal dentate gyrus of Tet1-TG mice. In addition, Tet1 overexpression induced the elevated expression of immediate early genes, such as Egr1, c-fos, Arc, and Bdnf, followed by the activation of intracellular calcium signals in prefrontal and hippocampal neurons.
mRNA expression in trophoblast cell populations from embryonic (E) day 8.5 to E12.5, including in progenitor and differentiated cells; expression restricted to specific trophoblast giant cell subtypes by late gestation (E14.5-E18.5)
The down-regulation of TET1 relieves its repression of the methylated Lhb gene promoter, which is then hydroxymethylated and activated by TET2 for full reproductive competence.
Tet1 deficiency is associated with hypermethylation of a subset of ICRs in germ cells.
e results showed mTet1 modified mGSCs had better self-renewal and proliferation ability than wild-type mGSCs, mTet1 could also up-regulate JMJD3 to decrease H3K27me3, which also showed to suppress the MEK-ERK pathway. Furthermore, Co-IP analysis demonstrated that TET1 interact with PCNA and HDAC1 by forming protein complexes to comprehensively regulate dairy goat mGSCs and spermatogenesis.
Iron(II)/alpha-Ketoglutarate-Dependent Catalytic Domains of the TET Enzymes
Tet1/2/3 proteins have a key role in modulating Wnt signaling and establishing the proper balance between neural and mesodermal cell fate determination in mouse embryos and embryonic stem cells
TET1 and TET2 play an important role in the proliferation of neural stem cells in the adult mouse brain.
findings reveal a novel role for TET1, an enzyme important for DNA hydroxymethylation, in the brain's reward circuitry in modulating stress responses in mice. Also identify a subset of genes that are regulated by TET1 in this circuitry.
These findings suggest that the catalytic and scaffolding activities of TDG are essential for retinoic acid-dependent gene expression and provide important insights into the mechanisms underlying targeting of TET-TDG complexes.
these results indicate that miR-29 is a direct regulator of Tet1 in mouse ESCs
a mechanism how L1 elements get activated in the absence of Mecp2
Nanog, Oct4 and Tet1 interplay in establishing stem cell pluripotency has been described.
that Tet1 modulates HIF-2alpha and HIF-1alpha through different mechanisms.
TET3 dioxygenase was present in the very first embryo stages, in contrast to TET1 and AICDA.
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