Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genomic BRD8-binding sites in human colorectal cancer cells

ABSTRACT: Genomic BRD8-binding sites in human colorectal cancer cells

PROVIDER: PRJNA841597 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19359216_1.fastq.gz	Fastqsanger.gz
	SRR19359216_2.fastq.gz	Fastqsanger.gz
	SRR19359217_1.fastq.gz	Fastqsanger.gz
	SRR19359217_2.fastq.gz	Fastqsanger.gz
	SRR19359218_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Genomic BRD8-binding sites in human colorectal cancer cells

Project description:Although BRD8 has been considered to act as a coactivator of the NuA4/TIP60-histone acetyltransferase complex, the role of BRD8 in colorectal cancer cells remains to be elucidated. We explored genomic BRD8-binding sites in human colorectal cancer cells.

2023-03-31 | GSE203615 | GEO

The effect of depletion of BRD8 or TIP60 on gene expression in colorectal cancer cells

Project description:Although BRD8 has been considered to act as a coactivator of the NuA4/TIP60-histone acetyltransferase complex, the role of BRD8 in colorectal cancer cells remains to be elucidated. We performed transcriptome analysis to identify BRD8- and TIP60-regulated genes in colorectal cancer cells.

2023-03-31 | GSE203236 | GEO

The Bromodomain Containing 8 (BRD8) Transcriptional Network in Human Lung Epithelial Cells [RNA-Seq]

Project description:Mechanisms regulating gene expression in the airway epithelium underlie its response to the environment. A network of transcription factors (TFs) and architectural proteins, modulate chromatin accessibility and recruit activating or repressive signals. Bromodomain-containing proteins function as TFs or by engaging methyltransferase or acetyltransferase activity to induce chromatin modifications. Here we investigate the role of Bromodomain Containing 8 (BRD8) in coordinating lung epithelial function. Sites of BRD8 occupancy genome-wide were mapped in human lung epithelial cell lines (Calu-3 and 16HBE14o-). CCCTC-Binding Factor (CTCF) was identified as a predicted co-factor of BRD8, based upon motif over-representation under BRD8 ChIP-seq peaks. Following siRNA-mediated depletion of BRD8, differentially expressed genes with peaks of BRD8 occupancy within 20 kb were subject to gene ontology process enrichment analysis. BRD8 targets are enriched for genes involved in the innate immune response and depletion of BRD8 increased the secretion of the antimicrobial peptide beta-defensin 1 and multiple chemokines.

2021-01-29 | GSE158678 | GEO

The Bromodomain Containing 8 (BRD8) Transcriptional Network in Human Lung Epithelial Cells [ChIP-seq]

2021-01-29 | GSE158686 | GEO

CUT&RUN profiling of genomic BFD1 binding sites

Project description:CUT&RUN profiling of genomic BFD1 binding sites

| PRJNA580219 | ENA

Identification of Esg genomic binding sites in Drosophila testes

Project description:Identification of Esg genomic binding sites in Drosophila testes

| PRJNA662382 | ENA

In vitro, genomic context identification of transcription factor binding sites

Project description:In vitro, genomic context identification of transcription factor binding sites

| PRJNA257554 | ENA

In vivo binding of PRDM9 reveals interaction with non-canonical genomic sites

Project description:In mouse and human meiosis, DNA double strand breaks (DSBs) initiate homologous recombination and occur at specific sites called hotspots. The localization of these sites is determined by the sequence specific DNA binding domain of the PRDM9 histone methyl transferase. Here we performed an extensive analysis of PRDM9 binding in mouse spermatocytes. Unexpectedly, we identified a non-canonical recruitment of PRDM9 to sites which are devoid of both, recombination activity and the PRDM9-binding consensus motif. These sites include transcription promoters, where PRDM9 is recruited in a DSB-dependent manner. Another subset of non-canonical sites also reveals DSB-independent interactions between PRDM9 and genomic sites, which include binding sites for the insulator protein CTCF. We propose that these DSB-independent sites result from interactions between hotspot bound PRDM9 and genomic sequences located on the chromosome axis.

2017-02-08 | GSE93955 | GEO

Alteration of genomic TERT-binding sites by BIBR1532 in primary neurons

Project description:Alteration of genomic TERT-binding sites by BIBR1532 in primary neurons

| PRJNA720830 | ENA

Alteration of genomic TERT-binding sites by BIBR1532 in primary neurons

Project description:The goal of this study is to understand how the specific TERT inhibitor BIBR1532 preconditioning regulates transcriptional reprogramming in mouse neuronal cells. We use CUT-Tag approach to comprehensively map the genomic binding sites of TERT in primary neurons and determine the alteration of is binding profile after BIBR1532 preconditioning. By obtaining over 10 million reads per sample, we generated genome-wide TERT chromatin-binding maps of mouse primary neurons. Under normal conditions, we show that more than 50% of the TERT binding sites were located at the promoter regions, many of them are previously unknown genomic loci. Intriguingly, BIBR1532 preconditioning significantly alters TERT-chromatin binding profile. Out of the total promoter binding sites by TERT, 30.4% (2,837 peaks) and 31.7% (2,954 peaks) are respectively upregulated and downregulated in TERT-binding after BIBR1532 preconditioning. Interestingly, we find that BIBR1532-preconditioned neurons show significant upregulation of promoter binding of TERT to the mitochondrial antioxidant genes. Together, these results identify the previously unknown TERT-binding sites in the mouse primary neurons and demonstrate that BIBR1532 preconditioning confers neuronal ischemic tolerance through TERT-mediated transcriptional reprogramming.

2021-09-28 | GSE171762 | 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