Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-Seq for transcriptional regulators and RNA Polymerase II in tumor cells treated with JQ1

ABSTRACT: ChIP-Seq of RNA Polymerase II, and transcriptional regulators in multiple myeloma (MM.1S), glioblastoma (U87-MG), and small cell lung carcinoma (H2171) treated with the BET bromodomain inhibitor JQ1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE49224 | GEO | 2013/07/26

SECONDARY ACCESSION(S): PRJNA213310

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ChIP-Seq for transcriptional regulators and RNA Polymerase II in tumor cells treated with JQ1

Project description:ChIP-Seq of RNA Polymerase II, and transcriptional regulators in multiple myeloma (MM.1S), glioblastoma (U87-MG), and small cell lung carcinoma (H2171) treated with the BET bromodomain inhibitor JQ1. Cell lines (MM.1S, U87-MG, and H2171) representing multiple myeloma, glioblastoma, and small cell lung carcinoma, were treated with varying concentrations (5nM to 5µM) of the BET bromodomain inhibitor JQ1 followed by ChIP-Seq for RNA Polymerase II and transcriptional regulators. Other datasets from this series of experiments have been release as a part of GSE42355.

2013-07-26 | E-GEOD-49224 | biostudies-arrayexpress

Small-molecule inhibitor JQ1 effect on multiple myeloma cell lines

Project description:Pathologic activation of c-Myc plays a central role in pathogenesis of several neoplasias, including multiple myeloma. However, therapeutic targeting of c-Myc has remained elusive due to its lack of a clear ligand-binding domain. We therefore targeted c-Myc transcriptional function by another means, namely the disruption of chromatin-dependent signal transduction. Members of the bromodomain and extra-terminal (BET) subfamily of human bromodomain proteins (BRD2, BRD3 and BRD4) associate with acetylated chromatin and facilitate transcriptional activation by increasing the effective molarity of recruited transcriptional activators. Notably, BRD4 marks select M/G1 genes in mitotic chromatin for transcriptional memory and direct post-mitotic transcription, via direct interaction with the positive transcription elongation factor complex b (P-TEFb). Because c-Myc is known to regulate promoter-proximal pause release of Pol II, also through the recruitment of P-TEFb, we evaluated the selective small-molecule inhibitor of BET bromodomains, JQ1, as a chemical probe to interrogate the role of BET bromodomains in Myc-dependent transcription and to explore their role as therapeutic targets in c-Myc-driven neoplasias. Duplicate cultures of MM.1S, OPM1 and KMS11 human myeloma cells were treated with either DMSO alone or with JQ1 (500 nM), for 24 hours. Total RNA was extracted and hybridized to Affymetrix human Gene 1.0 ST microarrays (two arrays per treatment per cell line for a total of 12 arrays).

2011-09-01 | E-GEOD-31365 | biostudies-arrayexpress

Differential gene expression in neuroblastoma cells after treatment with JQ1, nanaomycin, or combination of JQ1 and nanaomycin

Project description:BET bromodomain inhibitors are emerging as very promising novel anticancer agents. Combination of BET bromodomain inhibitor JQ1 and quinone-containing compound nanaomycin exerts synergistic anticancer effect in neuroblastoma We analysed whether a treatment with BET bromodomain inhibitor JQ1, and quinone-containing compound Nanaomycin synergistically modulate gene expression

2016-12-31 | GSE76066 | GEO

Gene expression profiling of MYC-amplified medulloblastoma cell lines treated by JQ1, a BET bromodomain inhibitor

Project description:MYC-amplified medulloblastomas are highly lethal tumors. BET bromodomain inhibition was recently described to downregulate MYC-associated transcriptional activity in various cancer subtypes. To investigate whether JQ1, a BET bromodomain inhibitor is downregulation MYC and MYC-associated transcriptional activity, we performed global gene expression profiling of five medulloblastomas MYC-amplified patient-derived cell lines treated by JQ1 and the inactive form of JQ1. Five medulloblastomas patient-derived MYC-amplified cell lines were treated with the active and the inactive form of the drug (JQ1S or JQ1R, respectively, 1μM for 24 hours) followed by RNA extraction and hybridization on Affymetrix microarrays

2013-12-02 | E-GEOD-51020 | biostudies-arrayexpress

Gene expression profiling of MYC-amplified medulloblastoma cell lines treated by JQ1, a BET bromodomain inhibitor

2013-12-02 | GSE51020 | GEO

Testis Gene Expression Changes after JQ1 treatment

Project description:JQ1 is a small-molecule (BET family) bromodomain inhibitor that causes a contraceptive effect in mice by blocking spermatogenesis and reducing sperm motility.

2012-08-16 | GSE37894 | GEO

Gene expression change after JQ1 treatment in breast cancer cell

Project description:BET bromodomain inhibitors effectively kill several types of cancer cells. However, the underlying mechanism of BET inhibition resistance remains obscure. We sought to identify the gene expression change upon treatment of JQ1, a well-known BET inhibitor, in basal-like breast cancer cells. In this dataset, we used RNA-sequencing to characterize the mRNA expression profiles from DMSO and JQ1-treated MDA-MB-231 breast tumor cells.

2019-11-07 | GSE140003 | GEO

Expression data from non-small cell lung cancer cell line DV90 after Bromodomain and extra terminal domain (BET) inhibitor JQ1 treatment

Project description:Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites resulting in changes in the transcription of specific genes. We used microarray profiling to investigate the transcriptional changes induced by BET inhibitor JQ1 treatment in DV90 cells to identify the underlying changes of gene regulation that lead to JQ1 sensitivity. DV90 cells (JQ1 sensitive non-small cell lung cancer cell line) were treated with 135 nM (IC50) or 785 nM (IC90) of JQ1 for 4h and 24h. DMSO treated controls served as reference and at least four replicates per condition were collected. RNA was extracted and hybridized to Affymetrix HuGene-2.1ST microarrays to identify treatment induced transcriptional changes.

2016-03-31 | E-GEOD-75960 | biostudies-arrayexpress

Gene expression signature of the T-ALL cell line LOUCY treated with 250nM (+)-JQ1 for 4h

Project description:We analyzed the transcriptional consequences of the BET bromodomain inhibitor JQ1 in the T-ALL cell line LOUCY by microarray analysis. Short-term exposure to a low dose of JQ1 (4h, 250nM) provided insights in the genes whose expression was immediately affected by BET bromodomain inhibition. Significantly downregulated genes upon short-term drug treatment included stem-cell associated genes and putative oncogenes such as BAALC, WT1, MN1, MEF2C, LMO1 and LMO2. Genes associated with the 500 highest ranked enhancer regions in LOUCY, were significantly enriched in genes downregulated after JQ1 treatment.

2016-12-15 | GSE81915 | GEO

Effect of BET bromodomain inhibition with JQ1 in stressed human derived iPS cardiomyocytes

Project description:Gene expression profile of endothelin-1 (ET-1) stressed human derived iPS cardiomyocytes (from Cellular Dynamics) with or without the BET bromodomain inhibitor JQ1

2017-03-30 | GSE96560 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data