Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differentially expressed genes in cells expressing WT or phospho-inactivating mutant (AA) BRD4

ABSTRACT: In this experiment, we use RNA-seq to examine the differentially expressed genes in DU145 and PC3 cells expressing WT (BRD4-WT) or phospho-inactivating mutant BRD4 (BRD4-AA)

ORGANISM(S): Homo sapiens

PROVIDER: GSE289083 | GEO | 2026/09/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

anti-Flag, anti-H3K4me3 and anti-H3K27ac Cut&Run on DU145 cells with endogenous BRD4 knockout and re-introduced of Flag-tagged WT- or AA-BRD4

Project description:In this experiment, we performed anti-Flag, anti-H3K4me3 and anti-H3K27ac Cut&Run on DU145 cells with endogenous BRD4 knockout and re-introduced of Flag-tagged WT- or AA-BRD4.

2026-09-28 | GSE276952 | GEO

IDR-Targeting Compounds Suppress HPV Genome Replication via Disruption of Phospho-BRD4 Association with DNA Damage Response Factors

Project description:Perturbation of genome-wide expression profiles and BRD4 isoform (BRD4-L and BRD4-S) binding by phospho-BRD4-targeting compounds (pNPS14, pNPS90, or pNPS145) or BET bromodomain inhibitor JQ1 in proliferating and differentiated W12E human cervical keratinocytes

2023-12-15 | GSE228786 | GEO

BRD4 ChIP-seq and CUT&RUN on DU145 cells treated with CDK2 inhibitor Tegtociclib (PF-07104091) or with cyclin E1 overexpression

Project description:In this experiment, we performed BRD4 ChIP-seq on DU145 cells upon CDK2 inhibition by Tegtociclib (also known as PF-07104091, a CDK2 inhibitor developed by Pfizer). We also performed BRD4 CUT&RUN on cyclin E1-overexpressing DU145 cells.

2026-09-28 | GSE241291 | GEO

BRD4 binding sites in transformed fibroblasts

Project description:Analysis of BRD4 ChIP-seq data of two types of human transformed fibroblasts (WT and HGPS) to identify specific and common binding sites for BRD4. Transformed cell lines were obtained by retroviral introduction of TERT (T), V12-HRAS (R) and SV40 large and small T antigens (S) of primary skin fibroblasts for HGPS patients (TRS-HGPS) and age-matched control wild-type individuals (TRS-WT) Abstract: Advanced age and DNA damage accumulation are strong risk factors for cancer. The premature-aging disorder Hutchinson Gilford Progeria Syndrome (HGPS) provides a unique opportunity to study the interplay between DNA damage and aging-associated tumor mechanisms, since HGPS patients do not develop tumors despite elevated levels of DNA damage. Here, we have used HGPS patient cells to identify a protective mechanism to oncogenesis. We find that HGPS cells are resistant to neo-plastic transformation. This resistance is mediated by the bromodomain protein BRD4, which exhibits altered genome-wide binding patterns in transformation-resistant cells leading to inhibition of oncogenic de-differentiation. BRD4 also in-hibits, albeit to a lower extent, the tumorigenic potential of transformed cells from healthy individuals and BRD4-mediated tumor protection is clinically relevant, since a BRD4 gene signature predicts positive clinical outcome in breast and lung cancer. Our results demonstrate a protective function for BRD4 and suggest tissue-specific functions for BRD4 in tumorigenesis. Examination of BRD4 binding events in TRS-WT and TRS-HGPS fibroblasts (2 independent cell lines in each group)

2014-10-02 | E-GEOD-61325 | biostudies-arrayexpress

iCLIP Analysis of WT, phospho-defective, and phospho-mimicking mutants of mouse Nucleolin in iKras PDAC cells

Project description:This experiment aimed to identify Nucleolin (Ncl) binding sites on a transcriptome-wide scale, by performing iCLIP in mouse iKras PDAC cells (Ying et al., 2012) transiently transfected with a mammalian expression construct encoding a wild-type (WT) myc-Ncl, a phospho-defective mutant in which S28, S34, S40, and S41 residues were mutated to A, or a phospho-mimicking mutant with these residues mutated to D. Cells transfected with an empty vector (myc-pRK5-DEST) were used as controls in the experiment.

2023-03-01 | E-MTAB-12481 | biostudies-arrayexpress

Brd4 knockout colonic epithelial organoids are partially resistant to IFNg-induced cell death.

Project description:To identify the role of Brd4 in colorectal cancer (CRC) development , we performed Sleeping Beauty (SB) transposon mutagenesis in mice. We identified several candidate genes including Brd4. To provide functional validation, we knocked out Brd4 in mouse tumor organoids carrying an activating KrasG12D, and an inactivating ApcD716 allele, and performed RNAseq. Brd4 knockout colonic organoids showed deregulation of genes in IFNg signaling. We treated Brd4 knockout organoids with IFNg and found that Brd4 konckout organoids showed partial resistance to IFNg-induce cell death. The mechanism may explain the function of Brd4 in colon cancer development.

2024-11-24 | GSE248821 | GEO

The proteome landscape of extracellular vesicles from prostate cancer cell lines

Project description:Proteome of extracellular vesicles (EVs) collected from prostate cancer cell lines - LNCaP, 22RV1, LNCaP 95, C4-2, DU145, PC3, NCI-H660, LASCPC-01, EF1.

2024-11-25 | MSV000096519 | MassIVE

iCLIP Analysis of WT, phospho-defective, and phospho-mimicking mutants of mouse Nucleolin in iKras PDAC cells

Project description:iCLIP Analysis of WT, phospho-defective, and phospho-mimicking mutants of mouse Nucleolin in iKras PDAC cells

| PRJEB58806 | ENA

Long non-coding RNA MANCR is a target of BET bromodomain protein BRD4 and plays a critical role for cellular migration and invasion abilities of prostate cancer

Project description:Androgen receptor (AR)-negative castration-resistant prostate cancer (CRPC) is highly aggressive and resistant to current therapies. BET bromodomain protein BRD4 binds to super-enhancers (SEs) that drive high expression of oncogenes in many cancers. A BET inhibitor JQ1 has been found to suppress malignant phenotypes of prostate cancer cells, however, the target genes of JQ1 remains largely unknown. Here we show that SE-associated genes specific for AR-negative CRPC PC3 cells include the genes involved in migration and invasion and that JQ1 impairs migration and invasion of PC3 cells. We identified the long non-coding RNA MANCR, which is markedly down-regulated by JQ1 and found that BRD4 binds to the MANCR locus. MANCR knockdown led to a significant decrease in migration and invasion of PC3 cells. RNA sequencing analysis revealed that expression of the genes involved in migration and invasion is altered by MANCR knockdown. In summary, our data demonstrate that MANCR has a critical role for cellular migration and invasion abilities of PC3 cells.

2020-03-23 | GSE145081 | GEO

IDR-Targeting Compounds Suppress HPV Genome Replication via Disruption of Phospho-BRD4 Association with DNA Damage Response Factors

Project description:IDR-Targeting Compounds Suppress HPV Genome Replication via Disruption of Phospho-BRD4 Association with DNA Damage Response Factors

| PRJNA951631 | ENA

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