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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 Antibodies (105) and many more products for this protein.
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We confirm the negative prognostic impact imparted by ASXL1 (show ASXL1 ELISA Kits) mutations and suggest a favorable impact from TET2 mutations in the absence of ASXL1 (show ASXL1 ELISA Kits) mutations.
TET2 mutation occurred in a number of ATLL patients and was likely involved in their leukemogenesis.
TET2 expression is reduced in myelodysplatic syndrome/acute myeloid leukemia (show BCL11A ELISA Kits) patients, independently of mutational status.
CD34 (show CD34 ELISA Kits)(+) cells lowering expression of TET2 may play an oncogenic role on myeloid tumor and CD3 (show CD3 ELISA Kits)(+) T cells of myelodysplastic syndrome patients may be derived from the malignant clone.
inactivation of MLL3 and TET2 may play an important role in the tumorigenesis process of HTLV-I-induced acute adult T-cell leukemia.
5-methylcytosine (5-hmC) expression is decreased in esophageal squamous cell carcinoma tissues, and is associated with TET2 expression level; TET2 reduction and subsequent 5-hmC loss might affect ESCC development
Among 864 Dutch persons between 80 and 105.8 years of age, DNA sequence analysis of TET2 confirmed a high incidence of somatic mutations but no effect on 10-year survival.
Mutations in TET2 gene is associated with cutaneous T cell lymphoma and Sezary syndrome.
Data show that tet methylcytosine dioxygenase 2 TET2, isocitrate dehydrogenases 1/2 IDH1 (show IDH1 ELISA Kits)/IDH2 (show IDH2 ELISA Kits), serine/arginine-rich splicing factor 2 SRSF2 (show SRSF2 ELISA Kits), splicing factor 3b subunit 1 SF3B1 (show SF3B1 ELISA Kits), and ras proteins (KRAS/NRAS) are not conserved in dog mast Cell tumors.
Here, the authors reveal the methylcytosine dioxygenases TET1 and TET2 as active regulators of CTCF (show CTCF ELISA Kits)-mediated alternative splicing through conversion of 5-methylcytosine to its oxidation derivatives.
Reprogramming of spermatogonial stem cells from Tet1 and Tet2 double knockout mice however lacked demethylation of H19 (show NCKAP1 ELISA Kits) imprinting control regions.
The critical roles of TET1/2 individually.
the stability of Foxp3 (show FOXP3 ELISA Kits) expression is markedly compromised in T reg (show KCNH2 ELISA Kits) cells from Tet2/Tet3 (show TET3 ELISA Kits) double-deficient mice.
Tet2 was responsible for increase in 5-hydroxymethylcytosine abundance after ischemic injury.
These results uncover the hypermethylation of DNA methylation (show HELLS ELISA Kits) canyons as the genomic key feature of Tet1/Tet2 double-knockout mouse embryonic fibroblasts.
our results indicate that neuronal TET2 is positively involved in the regulation of cell survival.
UNG (show UNG ELISA Kits) might be involved in Tet-mediated DNA demethylation.
Findings indicate a novel type of hematological malignancy induced by tet oncogene 2 protein (Tet2) loss.
Both TET1 and TET2 are required for the repression of embryonic stem cells differentiation by PRDM14.
reduced expression leads to Foxp3 (show FOXP3 ELISA Kits) hypermethylation and impairment of Treg-cell-associated immune homeostasis
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