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ChIP-Seq of transcriptional regulators in MM1S cells upon small molecule treatment.

ABSTRACT: Discovery of the genome-wide location of proteins using ChIP-Seq has allowed global mapping of the key transcription factors and chromatin regulators that control gene expression programs in various cells. Many DNA-associated processes are targeted for disease therapy. This study investigates the functions of small molecule therapeutics that target DNA-associated processes involved of CDK9 and BRD4.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43743 | GEO | 2013/12/13

SECONDARY ACCESSION(S): PRJNA187203

REPOSITORIES: GEO

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ChIP-Seq of transcriptional regulators in MM1S cells upon small molecule treatment.

Project description:Discovery of the genome-wide location of proteins using ChIP-Seq has allowed global mapping of the key transcription factors and chromatin regulators that control gene expression programs in various cells. Many DNA-associated processes are targeted for disease therapy. This study investigates the functions of small molecule therapeutics that target DNA-associated processes involved of CDK9 and BRD4. Genomic DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. ChIP was performed using an antibody against RNAP2, BRD4, CDK9, and CTCF using whole cell extract (WCE) as a background control.

2013-04-23 | E-GEOD-43743 | biostudies-arrayexpress

ChIP-Seq of Transcriptional Components in Ly1 DLBCL and Colon carcinoma

Project description:Discovery of the genome-wide location of proteins using ChIP-Seq has allowed global mapping of the key transcription factors and chromatin regulators that control gene expression programs in various cells. Many DNA-associated processes are targeted for disease therapy. This study investigates the functions of small molecule therapeutics that target DNA-associated processes involved with CDK9 and BRD4. Genomic DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. ChIP was performed using an antibody against Brd4, RNA Polymerase II, Med1, H3K27ac, and CDK8 as well as whole-cell extract (WCE) DNA controls

2013-12-24 | E-GEOD-53601 | biostudies-arrayexpress

ChIP-Seq of Transcriptional Components in Ly1 DLBCL and Colon carcinoma

2013-12-24 | GSE53601 | GEO

Chromatin occupancy of key transcriptional regulators in the presence of the BET bromodomain inhibitor JQ1

Project description:MM1.S cells are an aggressive dexamethasone sensitive multiple myeloma cell line whose transcritional program is driven by deregulated c-Myc activity. We present ChIP-seq analysis of key transcritional regulators that are implicated the c-Myc transcriptional network in MM1.S cells treated with vehicle or 500nM JQ1. Brd4, Cdk9, cMyc, Max, Med1, RNA Pol II, and the chromatin modifications H3K4me3 and H3K27Ac were profiled in MM1.S cells treated with 500nM JQ1 for 24hr

2012-11-30 | E-GEOD-42161 | biostudies-arrayexpress

Compensatory induction of MYC expression by sustained CDK9 inhibition via a BRD4-dependent mechanism: Pol II occupancy profiling by ChIP-Seq in HeLa cell line in the presence or absence of CDK9 inhibition

Project description:CDK9 is the kinase subunit of P-TEFb that enables RNA polymerase (Pol) II to transit from promoter-proximal pausing to productive elongation. Although considerable interest exists in CDK9 as a therapeutic target, little progress has been made due to the lack of highly selective inhibitors. Here, we describe the development of i-CDK9 as such an inhibitor that potently suppresses CDK9 phosphorylation of substrates and causes genome-wide Pol II pausing. While most genes experience reduced expression, MYC and other primary response genes increase expression upon sustained i-CDK9 treatment. Essential for this increase, the bromodomain protein BRD4 captures P-TEFb from 7SK snRNP to deliver to target genes and also enhances CDK9’s activity and resistance to inhibition. Because the i-CDK9-induced MYC expression and binding to P-TEFb compensate for P-TEFb’s loss of activity, only the simultaneous inhibition of CDK9 and MYC can efficiently induce growth arrest and apoptosis of cancer cells, suggesting the potential of a combinatorial treatment strategy. ChIP-seq of Pol II in HeLa cells before or after i-CDk9 treatment

2015-06-17 | E-GEOD-60953 | biostudies-arrayexpress

Expression profiling of HeLa cell line treated with CDK9 inhibitor

Project description:CDK9 is the kinase subunit of P-TEFb that enables RNA polymerase (Pol) II to transit from promoter-proximal pausing to productive elongation. Although considerable interest exists in CDK9 as a therapeutic target, little progress has been made due to the lack of highly selective inhibitors. Here, we describe the development of i-CDK9 as such an inhibitor that potently suppresses CDK9 phosphorylation of substrates and causes genome-wide Pol II pausing. While most genes experience reduced expression, MYC and other primary response genes increase expression upon sustained i-CDK9 treatment. Essential for this increase, the bromodomain protein BRD4 captures P-TEFb from 7SK snRNP to deliver to target genes and also enhances CDK9’s activity and resistance to inhibition. Because the i-CDK9-induced MYC expression and binding to P-TEFb compensate for P-TEFb’s loss of activity, only the simultaneous inhibition of CDK9 and MYC can efficiently induce growth arrest and apoptosis of cancer cells, suggesting the potential of a combinatorial treatment strategy. We used microarrays to examine the global impact on gene expression by imhibiting CDK9 at different time durations. HeLa cell lines treated with CDK9 inhibitor at different time points

2015-06-17 | E-GEOD-60952 | biostudies-arrayexpress

CDK9 inhibition with AZD4573 in DLBCL

Project description:We report the effects of CDK9 inhibition (AZD4573) on the epigenetic landscape in Diffuse Large B-cell Lymphoma (DLBCL). This study utilized chromatin immunoprecipitation with massively parallel DNA sequencing (ChIP-seq) to assess genome-wide post-translational histone modifications (H3K27ac and H3K4me3) and DNA occupancy of transcriptional proteins (RNAPII and BRD4) in two DLBCL cell lines, OCI-LY3 and VAL, treated with the CDK9 inhibitor AZD4573 (30 nM). Cells were treated for 0, 3 and 8 hours prior to harvest. After 8-hour exposure, drug was washed out and cells were harvested after 24 hours. We found that CDK9 inhibition led to an increase in RNAPII promoter proximal pausing, and increase in BRD4 enrichment on the promoter, and a decrease in promoter H3K4me3. Treatment induced reprograming of the super-enhancer landscape including loss of super-enhancers next to genes in oncogenic pathways.

2022-08-05 | GSE210372 | GEO

Functional analysis of the replication fork proteome identifies BET proteins as PCNA regulators

Project description:Identifying proteins that function at replication forks is essential to understand DNA replication, chromatin assembly, and replication-coupled DNA repair mechanisms. Combining quantitative mass spectrometry in multiple cell types with stringent statistical cutoffs, we generated a high confidence catalogue of 593 proteins that are enriched at replication forks and nascent chromatin. Loss of function genetic analyses indicate that 85% yield phenotypes consistent with activities in DNA and chromatin replication or already have described functions in these processes. We illustrate the value of this resource by identifying activities of the BET family proteins BRD2, BRD3, and BRD4 in controlling DNA replication. These proteins use their extra-terminal domains to bind and inhibit the ATAD5 complex and thereby control the amount of PCNA on chromatin.

2020-08-17 | PXD020914 | Pride

ChIP-Seq of Transcriptional Components in Colon carcinoma

Project description:Discovery of the genome-wide location of proteins using ChIP-Seq has allowed global mapping of the key transcription factors and chromatin regulators that control gene expression programs in various cells. Many DNA-associated processes are targeted for disease therapy. CDK8 is a kinase component of the Mediator co-activator complex and is often over-expressed in colorectal cancer. This study investigates the genome-wide localization of CDK8 in human colorectal cancer cells.

2013-12-24 | GSE53602 | GEO

ChIP-Seq of Transcriptional Components in Colon carcinoma

Project description:Discovery of the genome-wide location of proteins using ChIP-Seq has allowed global mapping of the key transcription factors and chromatin regulators that control gene expression programs in various cells. Many DNA-associated processes are targeted for disease therapy. CDK8 is a kinase component of the Mediator co-activator complex and is often over-expressed in colorectal cancer. This study investigates the genome-wide localization of CDK8 in human colorectal cancer cells. Genomic DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. ChIP was performed using an antibody against H3K27ac and CDK8 as well as whole-cell extract (WCE) DNA controls.

2013-12-24 | E-GEOD-53602 | biostudies-arrayexpress

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