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Bromodomain member BRD4 is required for hematopoietic stem cell functions (RNA-Seq)

ABSTRACT: To investigate the role of BRD4 in normal hematopoiesis, Brd4 conditional KO mouse model was generated. We purified the Lin-cKit+ cells from bone marrow of WT and Brd4 KO mice and performed the RNA-seq to study the molecular changes in each cell population.

ORGANISM(S): Mus musculus

PROVIDER: GSE189834 | GEO | 2023/08/20

REPOSITORIES: GEO

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Bromodomain member BRD4 is required for hematopoietic stem cell functions (ATAC-Seq)

Project description:To investigate the role of BRD4 in normal hematopoiesis, Brd4 conditional KO mouse model was generated. We purified the Lin-cKit+ cells from bone marrow of WT and Brd4 KO mice and performed the ATACseq to study the chromatin accessibility in each cell population.

2023-08-20 | GSE189832 | GEO

Bromodomain member BRD4 is required for hematopoietic stem cell functions (CUT&RUN)

Project description:To investigate the role of BRD4 in normal hematopoiesis, Brd4 conditional KO mouse model was generated. We purified the Lin-cKit+ cells from bone marrow of WT and Brd4 KO mice and performed the CUT&RUN to study the histone modification and Brd4 occupancy around genome in HSC/HPCs population.

2023-08-20 | GSE189833 | GEO

Bromodomain member BRD4 is required for hematopoietic stem cell functions (scRNA-Seq)

Project description:To investigate the role of BRD4 in normal hematopoiesis, Brd4 conditional KO mouse model was generated. We purified the cKit+ and LSK cells from bone marrow of WT and Brd4 KO mice and performed the single cell RNA-seq to study the molecular changes in each cell population.

2023-08-20 | GSE189835 | GEO

Bromodomain member BRD4 is required for hematopoietic stem cell functions

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-20 | GSE189836 | GEO

Ints11 is essential for normal function of hematopoietic stem/progenitor cells [RNA-seq]

Project description:To investigate the role of INTS11 in normal hematopoiesis, Ints11 conditional KO mouse model was generated. We purified the Lin-cKit+ cells from bone marrow of WT and Ints11 KO mice and studied the differentially expressed genes due to the Ints11 loss.

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Ints11 is essential for normal function of hematopoietic stem/progenitor cells [ChIP-Seq]

Project description:To investigate the role of INTS11 in normal hematopoiesis, Ints11 conditional KO mouse model was generated. We purified the Lin-cKit+ cells from bone marrow of WT and Ints11 KO mice and performed the ChIP-seq using different histone modifications to invesigate the gene regulation.

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Bromodomain protein BRD4 is required for estrogen receptor-dependent transcription and enhancer activation [ChIP-seq]

Project description:The estrogen receptor-α (ERα) is a transcription factor which plays a critical role in controlling cell proliferation and tumorigenesis by recruiting various cofactors to estrogen response elements (EREs) to induce or repress gene transcription. A deeper understanding of these transcriptional mechanisms may uncover novel therapeutic targets for ERα-dependent cancers. Here we show for the first time that BRD4 regulates ERα−induced gene expression by affecting elongation-associated phosphorylation of RNA Polymerase II (RNAPII P-Ser2) and histone H2B monoubiquitination (H2Bub1). Consistently, BRD4 activity is required for estrogen-induced proliferation of ER+ breast and endometrial cancer cells and uterine growth in mice. Genome-wide occupancy studies revealed an enrichment of BRD4 on transcriptional start sites as well as EREs enriched for H3K27ac and demonstrate a requirement for BRD4 for H2B monoubiquitination in the transcribed region of estrogen-responsive genes. Importantly, we further demonstrate that BRD4 occupancy correlates with active mRNA transcription and is required for the production of ERα-dependent enhancer RNAs (eRNAs). These results uncover BRD4 as a central regulator of ERα function and potential therapeutic target. ChIP-sequencing of BRD4, ERα and H2Bub1 in MCF7 cells treated with +/- estrogen treatment and or +/- JQ1 treatment in triplicates.

2014-07-10 | E-GEOD-55921 | biostudies-arrayexpress

Bromodomain protein BRD4 is required for estrogen receptor-dependent transcription and enhancer activation [RNA-Seq]

Project description:The estrogen receptor-M-NM-1 (ERM-NM-1) is a transcription factor which plays a critical role in controlling cell proliferation and tumorigenesis by recruiting various cofactors to estrogen response elements (EREs) to induce or repress gene transcription. A deeper understanding of these transcriptional mechanisms may uncover novel therapeutic targets for ERM-NM-1-dependent cancers. Here we show for the first time that BRD4 regulates ERM-NM-1M-bM-^HM-^Rinduced gene expression by affecting elongation-associated phosphorylation of RNA Polymerase II (RNAPII P-Ser2) and histone H2B monoubiquitination (H2Bub1). Consistently, BRD4 activity is required for estrogen-induced proliferation of ER+ breast and endometrial cancer cells and uterine growth in mice. Genome-wide occupancy studies revealed an enrichment of BRD4 on transcriptional start sites as well as EREs enriched for H3K27ac and demonstrate a requirement for BRD4 for H2B monoubiquitination in the transcribed region of estrogen-responsive genes. Importantly, we further demonstrate that BRD4 occupancy correlates with active mRNA transcription and is required for the production of ERM-NM-1-dependent enhancer RNAs (eRNAs). These results uncover BRD4 as a central regulator of ERM-NM-1 function and potential therapeutic target. mRNA expression profiles of MCF7 cells treated with +/- estrogen treatment under negative control siRNA, BRD4 siRNA or JQ1 treatment, in duplicates.

2014-07-10 | E-GEOD-55922 | biostudies-arrayexpress

The bromodomain protein BRD4 regulates splicing during heat shock

Project description:During heat stress cyto-protective genes including heat shock proteins are transcriptionally up-regulated and post-transcriptional splicing is inhibited. In contrast, co-transcriptional mRNA-splicing is maintained. These factors closely resemble the proteotoxic stress response during tumor development. The bromodomain protein BRD4 has been identified as an integral member of the oxidative stress as well as of the inflammatory response. Furthermore, there is evidence for BRD4's role in splicing regulation; Using RNA-Seq analyses we indeed found a significant increase in splicing inhibition, in particular intron retentions, during heat treatment in BRD4-deficient cells, but not under normal conditions. Subsequent experiments revealed that heat stress leads to the recruitment of BRD4 to nuclear stress bodies, to the interaction with the heat shock factor 1 (HSF1) and to the transcriptional up-regulation of non-coding Sat III RNA transcripts. These findings implicate BRD4 as a central regulator of splicing during heat stress. Since BRD4 is a potent target for anti-cancer therapies, our data linking BRD4 to the splicing machinery and the heat stress response - give additional insight into the mode of action of BRD4 inhibitors. WI38 cells have been treated by heatshock and anti BRD4 siRNA and combination.

2016-09-07 | E-GEOD-73471 | biostudies-arrayexpress

Bromodomain protein BRD4 is required for estrogen receptor-dependent transcription and enhancer activation [ChIP-seq]

2014-07-10 | GSE55921 | GEO

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