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Chromatin occupancy assessment an AML cell line treated with vehicle control, BETi, MDM2i, or a drug combination (BRD4-bound profiles)

ABSTRACT: Chromatin occupancy assessment an AML cell line treated with vehicle control, BETi, MDM2i, or a drug combination (BRD4-bound profiles)

PROVIDER: PRJNA546586 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9204740.fastq.gz	Fastqsanger.gz
	SRR9204741.fastq.gz	Fastqsanger.gz
	SRR9204742.fastq.gz	Fastqsanger.gz
	SRR9204733.fastq.gz	Fastqsanger.gz
	SRR9204743.fastq.gz	Fastqsanger.gz

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Chromatin occupancy assessment an AML cell line treated with vehicle control, BETi, MDM2i, or a drug combination (BRD4-bound profiles)

Project description:BRD4 chromatin occupancy changes in human OCI-AML3 cells treated with DMSO (vehicle control), the BET inhibitor CPI-203, the MDM2 inhibitor Nutlin-3a, or a combination of both drugs, were compared. Method: Genomic DNA from the OCI-AML3 cell line treated for 24 hrs with either DMSO, CPI-203, Nutlin-3a or a combination of both drugs was extracted, BRD4-bound chromatin was immunoprecipitated, then DNA was sequenced with an Illumina NextSeq 500 sequencer. Sequence reads passing the quality control filters were aligned using Bowtie2 and then analysed with SICER.

2020-11-04 | GSE132247 | GEO

Chromatin occupancy assessment an AML cell line treated with vehicle control, BETi, MDM2i, or a drug combination (p53-bound profiles)

Project description:Chromatin occupancy assessment an AML cell line treated with vehicle control, BETi, MDM2i, or a drug combination (p53-bound profiles)

| PRJNA546587 | ENA

Deep sequencing of an AML cell line treated with vehicle control, BETi, MDM2i, or a drug combination

Project description:Deep sequencing of an AML cell line treated with vehicle control, BETi, MDM2i, or a drug combination

| PRJNA546589 | ENA

Chromatin occupancy assessment an AML cell line treated with vehicle control, BETi, MDM2i, or a drug combination (p53-bound profiles)

Project description:p53 chromatin occupancy changes in human OCI-AML3 cells treated with DMSO (vehicle control), the BET inhibitor CPI-203, the MDM2 inhibitor Nutlin-3a, or a combination of both drugs, were compared. Method: Genomic DNA from the OCI-AML3 cell line treated for 24 hrs with either DMSO, CPI-203, Nutlin-3a or a combination of both drugs was extracted, p53-bound chromatin was immunoprecipitated, then DNA was sequenced with an Illumina NextSeq 500 sequencer. Sequence reads passing the quality control filters were aligned using Bowtie2 and then analysed with MACS.

2020-11-04 | GSE132246 | GEO

Deep sequencing of an AML cell line, with and without p53, treated with vehicle control, BETi, MDM2i, or a drug combination

Project description:Deep sequencing of an AML cell line, with and without p53, treated with vehicle control, BETi, MDM2i, or a drug combination

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BRD4 Chromatin immunoprecipitation and Sequencing

Project description:We report BET bromodomain inhibitors (BETi) as regulators of keratinocyte stem cell fate. BETi displace BET proteins, including BRD4 from chromatin, inducing acute transcriptional changes at selected target genes. To gain insight into the compound mechanism of action, we assayed BRD4 chromatin occupancy genome-wide in keratinocytes subjected to BETi treatment. Specifically, BRD4 chromatin binding was analyzed following two treatments [125nM (low) versus 1250nM (high)] and three time points (30min, 6h and 6h treatment followed by compound removal for 3h (6m3h)).

2020-10-15 | GSE130365 | GEO

BRD4 loading at the transcription start site mediates pause-release and underlies the disproportionate transcriptional response to BET bromodomain inhibition [RNA-Seq]

Project description:BET bromodomain inhibition (BETi) abrogates cancer cell growth by disrupting oncogenic gene expression. BRD4 loading at enhancers has been suggested to mediate pause-release and underlie the selective transcriptional response to BETi. Here, we utilized GRO-seq coupled with ChIP-seq to assess the association between gene control elements and the transcriptional response to BETi. Genes immediately down-regulated by BETi display a marked pause-release defect with a minimal impact on transcript elongation within the gene body. Surprisingly, we find that BRD4 at super-enhancers does not render its associated genes or enhancer RNAs preferentially sensitive to BETi. In contrast, disproportionate loading of BRD4 at transcription start sites (TSS) correlates with the transcriptional response to BETi. Moreover, BRD4 loading at TSSs, but not enhancers, is associated with enhanced promoter-proximal pausing following BETi. Our findings stress a mechanistic role of promoter-associated BRD4 in pause-release and suggest that BRD4 loading at the TSS drives the selective transcriptional response to BETi.

2023-01-06 | GSE70447 | GEO

BRD4 loading at the transcription start site mediates pause-release and underlies the disproportionate transcriptional response to BET bromodomain inhibition [GRO-Seq]

2023-01-06 | GSE70449 | GEO

BRD4 loading at the transcription start site mediates pause-release and underlies the disproportionate transcriptional response to BET bromodomain inhibition [ChIP-Seq]

2023-01-06 | GSE70448 | GEO

Deep sequencing of an AML cell line treated with vehicle control, BETi, MDM2i, or a drug combination

Project description:Gene expression changes in human OCI-AML3 cells treated with DMSO (vehicle control), the BET inhibitor CPI-203, the MDM2 inhibitor Nutlin-3a, or a combination of both drugs, were compared. Method: poly-A mRNA from the OCI-AML3 cell line treated for 24 hrs with either DMSO, CPI-203, Nutlin-3a or a combination of both drugs was extracted, in triplicate, then sequenced with an Illumina NextSeq500 sequencer. Sequence reads passing the quality control filters were aligned using Tophat2 and then analysed with Cufflinks.

2020-11-04 | GSE132244 | GEO

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