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The protein encoded by TET2 is a methylcytosine dioxygenase that catalyzes the conversion of methylcytosine to 5-hydroxymethylcytosine. Additionally we are shipping TET2 Kits (1) and many more products for this protein.
Showing 10 out of 136 products:
Human Monoclonal TET2 Primary Antibody for IP, WB - ABIN2668527
Wallner, Schröder, Leitão, Berulava, Haak, Beißer, Rahmann, Richter, Manke, Bönisch, Arrigoni, Fröhler, Klironomos, Chen, Rajewsky, Müller, Ebert, Lengauer, Barann, Rosenstiel, Gasparoni, Nordström et al.: Epigenetic dynamics of monocyte-to-macrophage differentiation. ... in Epigenetics & chromatin 2016
Show all 2 Pubmed References
Human Polyclonal TET2 Primary Antibody for IHC, ELISA - ABIN571057
Orr, Haffner, Nelson, Yegnasubramanian, Eberhart: Decreased 5-hydroxymethylcytosine is associated with neural progenitor phenotype in normal brain and shorter survival in malignant glioma. in PLoS ONE 2012
Human Polyclonal TET2 Primary Antibody for ELISA, IHC - ABIN4358584
Langemeijer, Kuiper, Berends, Knops, Aslanyan, Massop, Stevens-Linders, van Hoogen, van Kessel, Raymakers, Kamping, Verhoef, Verburgh, Hagemeijer, Vandenberghe, de Witte, van der Reijden, Jansen: Acquired mutations in TET2 are common in myelodysplastic syndromes. in Nature genetics 2009
Human Polyclonal TET2 Primary Antibody for ICC, IF - ABIN4358585
Fischer, Miles: Silencing HIF-1α induces TET2 expression and augments ascorbic acid induced 5-hydroxymethylation of DNA in human metastatic melanoma cells. in Biochemical and biophysical research communications 2017
TET2 in African Americans was associated with aggressive prostate cancer, with 24.4% of cases harboring a rare deleterious variant compared with 9.6% of controls
Therefore, chemical hypoxia not only causes overexpression of TET1 (show TET1 Antibodies) and TET2 but also could gradually do promoter demethylation of same genes
Overexpression of the wild-type TET1 (show TET1 Antibodies)/2/3 3'UTR (show UTS2R Antibodies) caused a significant increase in EZH2 (show EZH2 Antibodies) expression and tumor growth, whereas the mutation in miR (show MLXIP Antibodies)-26-binding sites abolished this effect.
Tet methylcytosine dioxygenase 2 (TET2) mutations can be detected in human MPhis cultured from MDS/CMML patient samples.
Concurrent STAT3 (show STAT3 Antibodies), DNMT3A (show DNMT3A Antibodies), and TET2 mutations in T-LGL leukemia with molecularly distinct clonal hematopoiesis of indeterminate potential
Multivariate analysis showed that KIT-AL and TET2 mutations were associated with inferior LFS, whereas age 40 years and marrow blast 70% were associated with inferior OS.
TET2- and TDG (show TDG Antibodies)-mediated changes are required for the acquisition of distinct histone modifications in divergent terminal differentiation of myeloid cells.
alterations in DNMT3A (show DNMT3A Antibodies) and TET2 may be associated with acute myeloid leukemia (show BCL11A Antibodies) prognosis
Mutation in the TET2 gene is associated with acute myeloid leukemia (show BCL11A Antibodies) patients with lympho-myeloid clonal hematopoiesis.
TET2-mutated haematopoietic precursor cells in Angioimmunoblastic T-cell lymphomas (AITLs) patients not only give rise to the T-cell lymphoma but also generate a large population of mutated mature B cells.
TET proteins, particularly TET2, were required for adipogenesis by modulating DNA methylation (show HELLS Antibodies) at the Ppargamma (show PPARG Antibodies) locus, subsequently by inducing Ppargamma (show PPARG Antibodies) gene expression.
Tet methylcytosine dioxygenase 2 (TET2) was the most highly expressed Tet enzyme in murine macrophage (MPhi) differentiation.
Here the authors show that concomitant loss of Tet2 and Tet3 (show TET3 Antibodies) in mice at early B cell stage blocked the pro- to pre-B cell transition in the bone marrow, decreased Irf4 (show IRF4 Antibodies) expression and impaired the germline transcription and rearrangement of the Igkappa locus.
in the absence of TET2, mast cell differentiation is under the control of compensatory mechanisms mediated by other TET family members, while proliferation is strictly dependent on TET2 expression.
ablation of Tet2 in myeloid cells suppresses melanoma growth in vivo and shifted the immunosuppressive gene expression program in tumor-associated macrophages to a proinflammatory one
These results support the hypothesis that somatic TET2 mutations in blood cells play a causal role in atherosclerosis.
Loss of TET2 expression is associated with development of malignancy.
confirm the transformation potential of DNMT3A (show DNMT3A Antibodies)(R882H) Tet2(-/-) progenitors and represent the first cooperative model in mice involving Tet2 inactivation driving lymphoid malignancies
indicate that AID and TET2 share common effects on myeloid and erythroid lineage differentiation, however, their role is nonredundant in regulating HSC (show FUT1 Antibodies) self-renewal and in myeloid transformation.
the results showed that low shear stress downregulated endothelial cell autophagy by impaired TET2 expression, which might contribute to the atherogenic process.
The protein encoded by this gene is a methylcytosine dioxygenase that catalyzes the conversion of methylcytosine to 5-hydroxymethylcytosine. The encoded protein is involved in myelopoiesis, and defects in this gene have been associated with several myeloproliferative disorders. Two variants encoding different isoforms have been found for this gene.
methylcytosine dioxygenase TET2
, probable methylcytosine dioxygenase TET2
, tet oncogene family member 2
, tet oncogene 2