Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wde mapping of BRD9 binding sites and gene expression changes upon BRD9 knockdown

ABSTRACT: Genome-wde mapping of BRD9 binding sites and gene expression changes upon BRD9 knockdown

PROVIDER: PRJNA531322 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8863350_1.fastq.gz	Fastqsanger.gz
	SRR8863350_2.fastq.gz	Fastqsanger.gz
	SRR8863351_1.fastq.gz	Fastqsanger.gz
	SRR8863351_2.fastq.gz	Fastqsanger.gz
	SRR8863346_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Genome-wde mapping of BRD9 binding sites and gene expression changes upon BRD9 knockdown

Project description:Leukemia is characterized by genetic and epigenetic mutations resulting in selection of cancer cells, which are unable to differentiate. While genetic alterations are difficult to target, the epigenome is intrinsically dynamic and readily offers new therapeutic strategies. Thus, identifying cancer-specific context-dependent targets and unraveling their biological function may open up new therapeutic perspectives. Here, we identify bromodomain-containing protein 9 (BRD9) as a critical target required in acute myeloid leukemia (AML). We show that BRD9 is overexpressed in AML cells including ex vivo primary blasts compared to CD34+ cells. By targeting BRD9 expression in AML, we observed an alteration in proliferation and survival, ultimately resulting in the induction of apoptosis. Intriguingly, genome-wide profiling revealed that BRD9 binds enhancer regions in a cell type-specific manner, regulating cell type-related processes. We unveil a novel BRD9-sustained STAT5 pathway activation via regulation of SOCS3 expression levels. Our findings identify a previously undescribed BRD9-STAT5 axis as critical for leukemia maintenance, suggesting BRD9 as a potential therapeutic target.

2019-05-02 | GSE129437 | GEO

HNF4G, AR, FOXA1, H3K4me1, H3K27acetyl binding sites upon knockdown and overexpression of HNF4G in 22Rv1 and LNCaP prostate cancer cells respectively

Project description:HNF4G is a gastrointestinal tissue enriched master transcriptional regulator seen overexpressed in a subset of prostate cancer. Here we have mapped binding sites of HNF4G, AR, Foxa1, H3K4me1, H3K27acetyl upon knockdown and overexpression of HNF4G in in 22Rv1 and LNCaP cells respectively

2017-11-01 | GSE85558 | GEO

Genome-wide binding of condesin upon SET1 knockdown

Project description:We reported the effect of condensin binding to the genome upon SET1 knockdown. ChIP-seq experiments of condensin (NCAPH2) were performed in control and SET1 knockdown cells. We found that condensin binding was significantly reduced upon SET1 knockdown.

2017-06-01 | GSE97540 | GEO

Baf250A, Brd9 and Baf180 knockdown impact on myoblast transcriptome

Project description:Baf250A, Brd9 and Baf180 knockdown impact on myoblast transcriptome

| PRJNA756240 | ENA

Baf250A, Brd9 and Baf180 knockdown impact on myoblast transcriptome

Project description:We performed RNA-seq to investigate global changes in gene expression in proliferating myoblasts transduced with either the scramble, Baf250A, Brd9 or Baf180 shRNAs. This study revelaed that the Baf250-containing BAF complex and the Brd9-containing ncBAF complex contribute to myoblast proliferation but the Baf180-containing PBAF subfamily does not.

2022-03-04 | GSE182421 | GEO

Transcriptome-wide mapping of RNA binding sites of the RNA-binding protein Unkempt using iCLIP-seq

Project description:iCLIP experiments tomap the RNA binding sites of the RNA-binding protein Unkempt across the transcriptome in SH-SY5Y cells, HeLa cells with ectopic Unk expression and mouse E15 embryonic brain samples. Expression of Unk is normally largely restricted to the nervous system. We therefore mapped the binding sites in human SH-SY5Y and mouse E15 brain to detect its physiological binding sites (in SH-SY5Y, we also performed the RNAseq experiment upon Unk knockdown). HeLa cells on the other hand normally don't express Unk, but convert to neuron-like shape when the protein is ectopically expressed. So, here we hoped to identify those binding events (and hence target transcripts) that are critical for this morphological transformation.

2015-03-09 | E-MTAB-2279 | biostudies-arrayexpress

The role of GABPA,GPD1L and BRD9 in renal cancer progression and metasasis

Project description:RNAseq was performed on the cells with GABPA knockdown, the cells with GPD1L knockdown, the cells with BRD9 knockdown and the control cells.

2022-05-18 | GSE165728 | GEO

Functional interplay between SWI/SNF complexes underlies BRD9 dependency in SMARCB1-mutant cancers [RNA-seq]

Project description:Genes encoding subunits of SWI/SNF (BAF) chromatin remodeling complexes are mutated in >20% of cancers. SWI/SNF complexes exist in three distinct families that each contribute to regulation of transcription, although the functional interactions between the families are not well understood. Rhabdoid tumors constitute an informative model system as these highly aggressive cancers are driven by inactivation of a single SWI/SNF subunit, SMARCB1, which is present in two SWI/SNF families (cBAF and PBAF) but not in the third (GBAF/ncBAF). We and others have shown that BRD9, a therapeutically targetable member of ncBAF, is essential specifically in SMARCB1-deficient cancers, suggesting key functional relationships between SMARCB1-containing complexes and BRD9/ncBAF. However, the mechanistic underpinnings of these relationships are poorly understood. Here, we demonstrate that genomic binding of BRD9 is largely dependent upon SMARCB1 such that the absence of SMARCB1 results in significantly reduced BRD9 binding. At select sites, however, we show that SMARCB1-loss results in gain of BRD9 binding and BRD9-dependent accessibility. We find that this gain is associated with expression of genes promoting cell migration. Our results define relationships between SWI/SNF complex families, elucidate mechanisms by which SMARCB1 loss drives oncogenesis, and provide mechanistic insight into the synthetic-lethal relationship between SMARCB1 and BRD9.

2023-07-14 | GSE210635 | GEO