Relevant bibliographies by topics / TET1 chromatin binding

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'TET1 chromatin binding'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "TET1 chromatin binding"

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Li, Wenjing, Violetta Karwacki-Neisius, Chun Ma, et al. "Nono deficiency compromises TET1 chromatin association and impedes neuronal differentiation of mouse embryonic stem cells." Nucleic Acids Research 48, no. 9 (2020): 4827–38. http://dx.doi.org/10.1093/nar/gkaa213.

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Abstract NONO is a DNA/RNA-binding protein, which plays a critical regulatory role during cell stage transitions of mouse embryonic stem cells (mESCs). However, its function in neuronal lineage commitment and the molecular mechanisms of its action in such processes are largely unknown. Here we report that NONO plays a key role during neuronal differentiation of mESCs. Nono deletion impedes neuronal lineage commitment largely due to a failure of up-regulation of specific genes critical for neuronal differentiation. Many of the NONO regulated genes are also DNA demethylase TET1 targeted genes. I
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Weng, Hengyou, Huilin Huang, He Huang, et al. "TET1 Modulates DNA Replication in Leukemia Cells Via a Catalytic-Independent Mechanism through Cooperating with KAT8." Blood 134, Supplement_1 (2019): 1249. http://dx.doi.org/10.1182/blood-2019-127321.

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TET1 was first identified as a fusion partner of the histone H3 Lys4 (H3K4) methyltransferase MLL (mixed-lineage leukemia) in acute myeloid leukemia (AML), and then was discovered as the founding member of the Ten-Eleven-Translocation (TET) family of DNA hydroxylases which are capable of converting 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). Our group has previously demonstrated that TET1 plays an oncogenic role in MLL-rearranged AML (Huang H, et al. PNAS 2013; 110(29):11994-9) and also other TET1-overexpressing AMLs (e.g., t(8;21) AML and AMLs carrying FLT3-ITD and/or NPM1 mutat
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Zhu, Xingguo, Caixia Xi, Alexander Ward та ін. "NRF2 mediates γ-globin gene regulation through epigenetic modifications in a β-YAC transgenic mouse model". Experimental Biology and Medicine 245, № 15 (2020): 1308–18. http://dx.doi.org/10.1177/1535370220945305.

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NRF2 is the master regulator for the cellular oxidative stress response and regulates γ-globin gene expression in human erythroid progenitors and sickle cell disease mice. To explore NRF2 function, we established a human β-globin locus yeast artificial chromosome transgenic/NRF2 knockout (β-YAC/NRF2−/−) mouse model. NRF2 loss reduced γ-globin gene expression during erythropoiesis and abolished the ability of dimethyl fumarate, an NRF2 activator, to enhance γ-globin transcription. We observed decreased H3K4Me1 and H3K4Me3 chromatin marks and association of TATA-binding protein and RNA polymeras
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Weng, Hengyou, Huilin Huang, Xi Qin, et al. "TET1 Regulates DNA Replication through Targeting of Minichromosome Maintenance Genes." Blood 128, no. 22 (2016): 2687. http://dx.doi.org/10.1182/blood.v128.22.2687.2687.

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Abstract DNA cytosine methylation is one of the best-characterized epigenetic modifications that play important roles in diverse cellular and pathological processes. The mechanism underlying the dynamic regulation of the level and distribution of 5-methylcytosine (5mC) as well as the biological consequence of DNA methylation deregulation have been interesting research topics in recent years. TET1, first identified as a fusion partner of the histone H3 Lys4 (H3K4) methyltransferase MLL (mixed-lineage leukemia) in acute myeloid leukemia (AML), is the founding member of the Ten-Eleven-Translocati
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Jiang, Xi, Chao Hu, Kyle Ferchen, et al. "Targeted Inhibition of STAT/TET1 Axis As a Potent Therapeutic Strategy for Acute Myeloid Leukemia." Blood 130, Suppl_1 (2017): 857. http://dx.doi.org/10.1182/blood.v130.suppl_1.857.857.

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Abstract Acute myeloid leukemia (AML) is one of the most common and fatal forms of hematopoietic malignancies. Over 70% of patients with AML cannot survive over 5 years. Many AML subtypes, such as the MLL -rearranged AMLs, are often associated with unfavorable outcome. Current treatment frequently involves intensive chemotherapy, which impairs the quality of life of the patients. While the incidence of AML is continually rising due to aging, most elder patients cannot bear intensive chemotherapy and are associated with very poor survival. Thus, improved therapeutic strategies with less intensi
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Masala, L., D. Bebbere, G. P. Burrai, et al. "210 DNA METHYLATION AND HYDROXYMETHYLATION ANALYSIS IN A MODEL OF OOCYTE DIFFERENTIAL DEVELOPMENTAL COMPETENCE IN SHEEP." Reproduction, Fertility and Development 27, no. 1 (2015): 195. http://dx.doi.org/10.1071/rdv27n1ab210.

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DNA methylation is an important epigenetic mark that plays a role in gene regulation by the addition of a methyl group to CpG islands in the DNA. Despite being relatively stable in somatic cells, DNA methylation is subject to reprogramming during embryo development and gametogenesis. The aim of this work was to evaluate different aspects of DNA methylation in relation to oocyte quality in the ovine species. A model of differential developmental competence consisting in ovine oocytes and in vitro produced (IVP) blastocysts derived from adult (AD) and prepubertal (PR) donors, was used. The methy
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Zhu, Xingguo, Alexander H. Ward, Caixia Xi та Betty S. Pace. "NRF2 Mediates Epigenetic Changes in DNA and Chromatin Structure to Regulate γ-Globin Gene Expression in a Human βYAC Transgenic Mouse Model". Blood 132, Supplement 1 (2018): 1053. http://dx.doi.org/10.1182/blood-2018-99-116438.

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Abstract NRF2 is the master regulator for the cellular anti-oxidative stress response and previously shown to activate γ-globin gene expression in human erythroid progenitor cells. The goal of this study was to expand on these findings by exploring the in vivo function of NRF2 using the human β-globin locus YAC transgenic (βYAC) mouse carrying the entire 248kb human β-globin locus (HBB). We observed that NRF2 activation by chronic dimethyl fumarate treatment of βYAC mice, induced human γ-globin gene expression, but had no effect on the adult β-globin gene. Subsequently in a novel βYAC/NRF2 kno
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8

Dolnik, Anna, Julia C. Engelmann, Maren Scharfenberger-Schmeer, et al. "Integrative Genomics Approaches Identify Novel Disease-Related Genetic Aberrations in Acute Myeloid Leukemia." Blood 118, no. 21 (2011): 402. http://dx.doi.org/10.1182/blood.v118.21.402.402.

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Abstract Abstract 402 Acute myeloid leukemia (AML) is a clonal disorder characterized by the accumulation of acquired somatic genetic alterations in hematopoietic progenitor cells that alter mechanisms of self-renewal, proliferation and differentiation. While recently numerous aberrations have been identified, many more mutations involved in the multistep pathogenesis of AML still remain to be discovered. Based on critical regions and differentially expressed genes identified by our SNP/aCGH and microarray-based gene expression profiling analysis of 320 AML cases, we designed a custom capture
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9

Lio, Chan-Wang J., Vipul Shukla, Daniela Samaniego-Castruita, et al. "TET enzymes augment activation-induced deaminase (AID) expression via 5-hydroxymethylcytosine modifications at the Aicda superenhancer." Science Immunology 4, no. 34 (2019): eaau7523. http://dx.doi.org/10.1126/sciimmunol.aau7523.

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TET enzymes are dioxygenases that promote DNA demethylation by oxidizing the methyl group of 5-methylcytosine to 5-hydroxymethylcytosine (5hmC). Here, we report a close correspondence between 5hmC-marked regions, chromatin accessibility and enhancer activity in B cells, and a strong enrichment for consensus binding motifs for basic region-leucine zipper (bZIP) transcription factors at TET-responsive genomic regions. Functionally, Tet2 and Tet3 regulate class switch recombination (CSR) in murine B cells by enhancing expression of Aicda, which encodes the activation-induced cytidine deaminase (A
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10

Cao, John Z., Hui Liu, Amittha Wickrema, and Lucy A. Godley. "HIF-1 directly induces TET3 expression to enhance 5-hmC density and induce erythroid gene expression in hypoxia." Blood Advances 4, no. 13 (2020): 3053–62. http://dx.doi.org/10.1182/bloodadvances.2020001535.

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Abstract In mammalian cells, cytosines found within cytosine guanine dinucleotides can be methylated to 5-methylcytosine (5-mC) by DNA methyltransferases and further oxidized by the Ten-eleven translocation dioxygenase (TET) enzymes to 5-hydroxymethylcytosine (5-hmC). We have previously shown that hematopoietic stem and progenitor cells (HSPCs) with TET2 mutations have aberrant 5-hmC distribution and less erythroid differentiation potential. However, these experiments were performed under standard tissue culture conditions with 21% oxygen (O2), whereas HSPCs in human bone marrow reside in ∼1%
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Dissertations / Theses on the topic "TET1 chromatin binding"

1

Pantier, Raphaël Pierre. "Molecular interactions of TET proteins in pluripotent cells." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31253.

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Ten-Eleven-Translocation (TET) proteins form a family of enzymes responsible for active DNA demethylation by oxidation of 5-methylcytosine. TET proteins play a key role in genomic reprogramming in vitro and in vivo. Although TET proteins are expressed in embryonic stem cells (ESCs), their role in regulating pluripotency remains unclear. In addition, the mechanisms by which TET proteins are recruited to chromatin are largely unknown. To visualise TET protein dynamics during pluripotency and differentiation, the endogenous Tet1/2/3 alleles were fused to epitope tags in ESCs using CRISPR/Cas9. Ch
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