Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of endothelial specific inhibition of Brg1

ABSTRACT: Effect of endothelial specific inhibition of Brg1

PROVIDER: PRJNA827589 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18779930_1.fastq.gz	Fastqsanger.gz
	SRR18779930_2.fastq.gz	Fastqsanger.gz
	SRR18779931_1.fastq.gz	Fastqsanger.gz
	SRR18779931_2.fastq.gz	Fastqsanger.gz
	SRR18779932_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Effect of endothelial specific inhibition of Brg1 on histone marker H3K4me3 in the zebrafish genome [ChIP-seq]

Project description:To decipher the effect of endothelial specific inhibition of Brg1 on histone marker H3K4me3 in the zebrafish genome during zebrafish heart regeneration, we achieved endothelium-specific over-expression of DN-xBrg1 by using the compound zebrafish line consisting of Tg(ubi:loxp-DsRed-STOP-loxp-DN-xBrg1; kdrl:CreER) (defined as DN), while we used Tg(ubi:loxp-DsRed-STOP-loxp-DN-xBrg1) as control (Ctrl) in the presence of 4-HT starting at 3 days before ventricular resection. The whole ventricles from CtrlK and DNK hearts at 7 dpa were subjected to ChIP-seq analysis using H3K4me3 antibody.

2023-04-03 | GSE200937 | GEO

Effect of endothelial specific inhibition of Brg1 on gene expression during zebrafish heart regeneration [RNA-seq]

Project description:Effect of endothelial specific inhibition of Brg1 on gene expression during zebrafish heart regeneration [RNA-seq]

| PRJNA827593 | ENA

Effect of endothelial specific inhibition of Brg1 on histone marker H3K4me3 in the zebrafish genome [ChIP-seq]

Project description:Effect of endothelial specific inhibition of Brg1 on histone marker H3K4me3 in the zebrafish genome [ChIP-seq]

| PRJNA827592 | ENA

Effect of endothelial specific inhibition of Brg1 on gene expression during zebrafish heart regeneration [RNA-seq]

Project description:To decipher the molecular action of endothelial Brg1 in the regulation of zebrafish heart regeneration, we applied Tg(kdrl:eGFP) to label cardiac endothelial cells including the endocardium, and achieved endothelium-specific over-expression of DN-xBrg1 by using the compound zebrafish line consisting of Tg(ubi:loxp-DsRed-STOP-loxp-DN-xBrg1; kdrl:CreER; kdrl:eGFP) (defined as DNK), while we used Tg(ubi:loxp-DsRed-STOP-loxp-DN-xBrg1; kdrl-eGFP) as control (CtrlK) in the presence of 4-HT starting at 3 days before ventricular resection. The kdrl:eGFP endothelial cells, which were sorted by FACS (fluorescence-activated cell sorting) from CtrlK and DNK hearts at 7 dpa, were subjected to RNA-seq analysis.

2023-04-03 | GSE200936 | GEO

Effect of ATM inhibition in primary endothelial cells

Project description:Effect of ATM inhibition in primary endothelial cells

| PRJNA589641 | ENA

Effect of endothelial specific inhibition of Brg1

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-04-03 | GSE200938 | GEO

LINC00607 is essential to maintain the endothelial phenotype through SWI/SNF chromatin remodeler BRG1

Project description:Long non-coding RNAs (lncRNAs) are regulatory RNAs, which by altering gene expression impact on the cellular phenotype and cardiovascular disease development. The pool of endothelial lncRNAs and their vascular function is largely undefined. Deep-endothelial RNA-Seq and FANTOM5 CAGE analysis revealed LINC00607 as a specifically enriched and highly expressed lncRNA in human endothelial cells. LINC00607 was induced in response to hypoxia, arteriosclerosis regression in non-human primates and also in response to propranolol used to induce regression of human arteriovenous malformations. siRNA Knockdown or CRISPR/Cas9 knockout of LINC00607 attenuated VEGF-A-induced angiogenic sprouting. LINC00607 knockout HUVEC also integrated less into newly formed vascular networks in an in vivo assay in SCID mice. Overexpression of LINC00607 in CRISPR knockout cells restored the normal function. RNA- and ATAC-Seq of the LINC00607 knockout revealed changes in transcription of endothelial gene sets particularly linked to the endothelial phenotype. This was most likely the consequence of a reduced chromatin accessibility of the ERG binding motif. Mechanistically, LINC00607 interacts with the SWI/SNF chromatin remodeling protein BRG1. CRISPR/Cas9-mediated knockout of BRG1 in HUVEC followed by CUT&RUN revealed that BRG1 is required to secure a stable chromatin state, mainly on ERG-binding sites. In conclusion, LINC00607 is a highly expressed endothelial-specific lncRNA important for efficient endothelial gene transcription through sustaining ERG target gene transcription by interaction with the chromatin remodeler BRG1.

2023-01-09 | GSE201824 | GEO

The effect of BRG1 on the responsivness of IFNg Stimulated Genes

Project description:We studied the effect of reconstitution of BRG1 in BRG1-deficient cells on the responsivness of IFNg stimulated genes. Cells were infected with control adenovirus or BRG1-encoding virus. Cells were then left untreated or exposed to IFNg for 6 hours. Total RNA was collected and analyzed with Illumina arrays. SW13 cells were infected with BRG1-encoding adenovirus or control virus. Cells were left untreated or exposed to IFNg for 6 hours

2015-05-01 | E-GEOD-67626 | biostudies-arrayexpress

Endothelial Brg1-Notch Signaling Regulates Zebrafish Heart Regeneration

Project description:Endothelial Brg1-Notch Signaling Regulates Zebrafish Heart Regeneration

| PRJNA645397 | ENA

Protein-protein interactions of BRG1 or BRG1-HSA in SW13 cells

Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.

2023-02-15 | PXD029647 | Pride

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