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Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

ABSTRACT: Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

PROVIDER: PRJNA788630 | ENA |

REPOSITORIES: ENA

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Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

Project description:Here we report both TET1-WT and catalytically dead mutant TET1 (TET1-MUT) directly interact with STAT5B in PDX2 B-ALL cells. To study the landscape of TET1 and STAT5B binding in whole genomic DNA and test if the STAT5B binding signal is affected by TET1, we conduct the ChIP-seq assay with flag antibody (TET1-WT, TET1-MUT) and STAT5B antibody (sgNS or sgTET1) respectively. The results showed that TET1 bound peaks overlap with STAT5B very well and the tag density of STAT5B on target genes decreases in TET1-impeded cells. We conclude that TET1 recruit STAT5B to the promoters of its target genes and further promote the target genes’ transcriptions.

2023-02-13 | GSE190852 | GEO

Global change of RNA expression upon silencing TET1 in PDX2 B-ALL cells Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

Project description:Global change of RNA expression upon silencing TET1 in PDX2 B-ALL cells Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

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Genome-wide maps of Tet1 binding in [WT, Tet1-Flag] and [Dnmt3a-/-, Tet1-Flag] J1 ES cells

Project description:In order to assess Tet1 binding, we first generated a Flag tagged Tet1 ES cells and then knocked out Dnmt3a in the [WT, Tet1-Flag] cells. By Tet1 ChIP and Flag ChIP, we showed that Tet1 binding was complementary to Dnmt3a. And Tet1 binding was not affected or slightly increased at majority of its targets.

2018-05-16 | GSE100955 | GEO

Prolactin-inducible Stat5a-mediated and Stat5b-mediated gene profiles

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Genome-wide maps of TET1 binding in mouse frontal cortex

Project description:With anti-TET1 immunoprecipitated chromatin from mouse frontal cortices, we generated TET1 binding maps with 4496 high-confidence peaks and approximately 90% of TET1 peaks were within intergenic regions.

2019-07-25 | GSE124671 | GEO

Prolactin-inducible Stat5a-mediated and Stat5b-mediated gene profiles

Project description:Stat5a and Stat5b proteins are highly homologous with greater than 90% amino acid identity and share binding to the palindromic Stat5 consensus sequence, TTCNNNGAA, but individual roles of each transcription factor in breast cancer have not been thoroughly evaluated. To determine the degree of similarity between transcripts modulated by Stat5a and Stat5b proteins in human breast cancer, we utilized genome-wide transcript profiling to identify genes regulated specifically by Stat5a or Stat5b in response to prolactin. Stat5a or Stat5b was transiently overexpressed using adenoviral gene delivery in MCF7 breast cancer cells followed 16 hr serum starvation and a brief 4 hr exposure to 10nM human prolactin to identify immediate-early transcripts modulated by each transcription factor. Basal activation of Stat5a or Stat5b was not present in cells not stimulated with prolactin. mRNA from each condition was harvested and validated using the Agilent bioanalyzer. cDNA was generated and genome-wide transcript profiling was performed in triplicate using the Affymetrix HuGene 1.0 ST array.

2012-08-29 | E-GEOD-37781 | biostudies-arrayexpress

The role of DNMT3A and TET1 in regulating promoter epigenetic landscapes

Project description:The role of DNMT3A and TET1 in regulating promoter epigenetic landscapes

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Genetic STAT5B immunodysregulatory disorder

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Genetic STAT5B immunodysregulatory disorder

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TET1 interactome in mESCs (via ChIP-MS)

Project description:Precise regulation of DNA methylation in mammals is critical for genome stability and epigenetic regulation. The discovery of the ten-eleven translocation (TET) proteins catalyzing the oxidation from 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC) revolutionized the perspective on the complexity and regulation of DNA modifications. Despite accumulating knowledge about the role of TET1, it remains unclear to what extent these can be attributed to its catalytic activity. Here, we use genome engineering and quantitative multi-omics approaches to dissect the role and mechanism of TET1 in mESCs. Our study identifies TET1 as an essential interaction hub for multiple chromatin modifying complexes and as a global regulator of histone modifications. Strikingly, we find that the majority of transcriptional regulation depends on non-catalytic functions of TET1. Moreover, we show that the establishment of H3K9me3 and H4K20me3 at ERV1, ERVK, and ERVL is mediated by TET1 independent of DNA demethylation. We provide evidence that repression of endogenous retroviruses depends on the interaction between TET1 and SIN3A. In summary, we demonstrate that the non-catalytic functions of TET1 are critical for regulation of gene expression and the silencing of endogenous retroviruses in mESCs.

2022-08-31 | PXD028850 | Pride

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