Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human TET1 Antibodies:
anti-Mouse (Murine) TET1 Antibodies:
anti-Rat (Rattus) TET1 Antibodies:
Go to our pre-filtered search.
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
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.
Infrequent occurrence of TET1, TET3, and ASXL2 mutations in myelodysplastic/myeloproliferative neoplasms.
the findings of this study indicate that miR27a3p is upregulated, while TET1 is downregulated in human osteosarcoma cells
TET1 gene expression might serve as a reliable predictor for patients survival in acute myeloid leukemia.
expressed in trophoblast cell columns of first-trimester placentas
Study provides evidence that low-expression of TET1 in oral squamous cell carcinoma (OSCC) stem cells may stimulate MGMT promoter methylation, while inhibiting MGMT mRNA expression, which ultimately strengthens the sensitivity of OSCC stem cells in regards to chemotherapeutics.
TET1 exerts its tumor suppressor function by regulating autophagy in glioma.
TET1 expression levels were significantly elevated in EGFR mutant samples (P=0.007). Patients with higher TET1 levels showed a trend of better response rates to EGFR inhibitors compared to low TET1 staining levels, although the result was not significant (P=0.08).
Although DNA methylation (5mC) and hydroxymethylation (5hmC) are highly dynamic during early embryonic development, less is known about their roles at later stages of differentiation. 5hmC marks HNF4A promoter 1 previous to terminal hepatocyte differentiation. TET1-dependent 5hmC is required to activate promoter 1-driven HNF4A expression.
Study comprehensively examined TET1 expression and methylation status in multiple tumors, and demonstrated that promoter CpG methylation is a predominant mechanism for TET1 inactivation in human cancers. TET1 as a tumor suppressor and CpG demethylase in tumor cells requires its intact catalytic domain, which provides new insight into the epigenetic master role of TET1 in tumor pathogenesis.
our findings demonstrate that 5-hmC loss is an epigenetic hallmark of hepatocellular carcinoma , and miR-29a is an important epigenetic modifier, promoting HCC metastasis through TET-SOCS1-MMP9 axis silencing. The results offer a new strategy for epigenetic cancer therapy
These results suggest that TET1 potentially promotes the cytodifferentiation potential of human dental pulp cells through its DNA demethylation machinery and upregulation of FAM20C protein expression.
a mechanism how L1 elements get activated in the absence of Mecp2
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
Nanog, Oct4 and Tet1 interplay in establishing stem cell pluripotency has been described.
that Tet1 modulates HIF-2alpha and HIF-1alpha through different mechanisms.
TET1 is an epigenetic determinant for regulating genes that are crucial to closure of the anterior neural tube.
Tet enzymes play important roles in telomere maintenance and chromosomal stability of embryonic stem cells by modulating sub-telomeric methylation levels.
MBD1 regulates localization and activity of Tet1 in a CXXC3 domain-dependent manner.
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.
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