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Mus musculus

ABSTRACT: Genome wide TFIIB binding during postnatal and pressure-induced cardiac hypertrophy

PROVIDER: PRJNA244672 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1238743.fastq.gz	Fastqsanger.gz
	SRR1238744.fastq.gz	Fastqsanger.gz
	SRR1238745.fastq.gz	Fastqsanger.gz
	SRR1238746.fastq.gz	Fastqsanger.gz

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Similar Datasets

Genome wide TFIIB binding during postnatal and pressure-induced cardiac hypertrophy

Project description:Purpose: To identify the differential TFIIB bindingl patterns during postnatal cardiac growth, pressure-induced cardiac hypertrophy and adult mouse hearts Methods: Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for TFIIB- ChIP-Seq. Results: In accordance with previosly published data (Sayed D, et. al. JBC, 2013 Jan 25;288(4):2546-58) with genome wide polII and H3K9ac status during cardiac hypertrophy (GSE50637), Denovo TFIIB recruitment was restricted to speclaized genes with cardiac hypertrophy. Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for TFIIB- ChIP-Seq.

2014-11-17 | E-GEOD-56813 | biostudies-arrayexpress

Genome wide TFIIB binding during postnatal and pressure-induced cardiac hypertrophy

2014-11-17 | GSE56813 | GEO

NelfA (Whsc2) promoter occupancy is required for active gene transcription during cardiac hypertrophy

Project description:We examineD the genomic oppucpany and role of negative elongation factor A (NelfA) aka, Wolf-Hirschhorn syndrome candidate 2 (Whsc2), a critical component of the negative elongation complex in hearts undergoing pressure-overload induced cardiac hypertrophy. Alignment of high resolution genome wide occupancy data of NelfA, RNA Pol II, TFIIB and H3k9ac (datasets for pol II, TFIIB and H3kac submitted before) from control and hypertrophied hearts reveal that NelfA associates with all active gene promoters. High NelfA occupancy is seen at promoters of essential and cardiac-enriched genes, expressed under both quiescent and hypertrophic conditions. Conversely, de novo NelfA recruitment is observed at inducible gene promoters with pressure overload, accompanied by significant increase in expression of latter genes with hypertrophy.

2020-05-19 | GSE135829 | GEO

Mus musculus

Project description:Pressure-Overload Induced Cardiac Hypertrophy

| PRJNA85517 | ENA

Transcriptional regulation patterns revealed by high-resolution chromatin immunoprecipitation during cardiac hypertrophy

Project description:Purpose: To identify the differential transcriptional patterns during postnatal cardiac growth, pressure-induced cardiac hypertrophy and adult mouse hearts Results: Our data revealed novel transcriptional patterns during cardiac growth conditions. The results showed that most of the essential genes are regulated by promoter clearance of paused RNA pol II, while de novo recruitment is required for regulation of mostly speclaized genes during cardiac growth. We have identified two major modes of gene regulation durign cardiac hypertrophy and four transcriptional growth patterns. The results are published in January 2013 issue of Journal of Biological Chemistry.

2013-09-06 | GSE50637 | GEO

Transcriptional regulation patterns revealed by high-resolution chromatin immunoprecipitation during cardiac hypertrophy

2013-09-06 | E-GEOD-50637 | biostudies-arrayexpress

Mus musculus

Project description:Pressure overload cardiac hypertrophy

| PRJNA92679 | ENA

Gene profiling of Hand2 target genes and transcriptional regulation of Hand2 expression in the postnatal myocardium

Project description:In humans, cardiac hypertrophy is the principal risk factor for the development of overt heart failure and sudden cardiac death from lethal arrhythmias. Although aberrant reactivation of fetal² gene programs is intricately linked to maladaptive hypertrophy of postnatal cardiomyocytes, loss of cardiac function and heart failure, the transcription factors driving these gene programs remain ill defined. We report that the basic helix-loop-helix (bHLH) transcription factor dHAND/Hand2 is re-expressed in the mammalian postnatal myocardium in response to stress signaling. Interestingly, mutant mice overexpressing Hand2 in otherwise healthy ventricular myocytes developed a phenotype of pathological hypertrophy. In contrast, conditional gene-targeted Hand2 mice demonstrated a marked resistance to pressure overload-induced hypertrophy, fibrosis, ventricular dysfunction and induction of a fetal gene program. These data suggest a critical role for the Hand2 transcription factor during hypertrophic remodeling and heart failure. To gain more mechanistically insight in the processes underlying heart failure, we here identified Hand2 target genes by microarray gene expression profiling. RNA samples were collected 4 weeks after sham or TAC surgery (to induce pressure overload) of both tamoxifen-treated Hand2f/f (WT) and MCM-Hand2f/f (KO) mice.

2013-11-15 | E-MTAB-1821 | biostudies-arrayexpress

Mus musculus

Project description:IL-18 and Pressure Overload-induced Cardiac Hypertrophy

| PRJNA96633 | ENA

Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

Project description:Pathological cardiac hypertrophy is a major risk factor for the development of heart failure and sudden cardiac death, yet the molecular mechanism of cardiac hypertrophy is not fully understood. Recently, we found that the expression of Lin28a, a RNA-binding protein, was significantly upregulated during the early stages of cardiac hypertrophy. Interestingly, cardiac specific conditional deletion of Lin28a blunted pressure overload-induced cardiac hypertrophic responses. Given that Lin28a can bind to diverse mRNA to regulate their abundance and/or translation, we conducted RNA-seq to profile the cardiac transcriptome alteration without Lin28a under pressure overload. It showed that metabolic pathways, including glycolysis and biosynthetic pathway, were remarkedly affected. Thus, our study identifies Lin28a as a crucial regulator of cardiac hypertrophy via its role in metabolic programming.

2019-04-30 | GSE106897 | GEO

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