Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide fetalization of enhancer architecture in heart disease [ChIP-Seq]

ABSTRACT: Genome-wide fetalization of enhancer architecture in heart disease [ChIP-Seq]

PROVIDER: PRJNA522418 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19348501.fastq.gz	Fastqsanger.gz
	SRR19348502.fastq.gz	Fastqsanger.gz
	SRR19348503.fastq.gz	Fastqsanger.gz
	SRR19348504.fastq.gz	Fastqsanger.gz
	SRR19348505.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 98

Similar Datasets

Genome-wide fetalization of enhancer architecture in heart disease

Project description:Genome-wide fetalization of enhancer architecture in heart disease

| PRJNA522393 | ENA

Genome-wide fetalization of enhancer architecture in heart disease [ChIP-Seq]

Project description:Heart disease is associated with re-expression of key transcription factors normally active only during prenatal development of the heart. However, the impact of this reactivation on the genome-wide regulatory landscape in heart disease has remained obscure. Here we show that pervasive epigenomic changes occur in heart disease, with thousands of regulatory sequences reacquiring fetal-like chromatin signatures. We used RNA-seq and ChIP-seq targeting a histone modification associated with active transcriptional enhancers to generate genome-wide enhancer maps from left ventricle tissue from 18 healthy controls and 18 individuals with idiopathic dilated cardiomyopathy (DCM). Healthy individuals had a highly reproducible epigenomic landscape, consisting of more than 31,000 predicted heart enhancers. In contrast, we observed reproducible disease-associated gains or losses of activity at more than 7,500 predicted heart enhancers. Next, we profiled human fetal heart tissue by ChIP-seq and RNA-seq. Comparison with adult tissues revealed that the heart disease epigenome and transcriptome both shift toward a fetal-like state, with more than 3,400 individual enhancers sharing fetal regulatory properties. Our results demonstrate widespread epigenomic changes in DCM, and we provide a comprehensive data resource (http://heart.lbl.gov) for the mechanistic exploration of heart disease etiology.

2019-04-02 | GSE126571 | GEO

Genome-wide fetalization of enhancer architecture in heart disease [RNA-Seq]

Project description:Genome-wide fetalization of enhancer architecture in heart disease [RNA-Seq]

| PRJNA522417 | ENA

Genome-wide fetalization of enhancer architecture in heart disease [RNA-Seq]

2019-04-02 | GSE126569 | GEO

Genome-wide fetalization of enhancer architecture in heart disease.

Project description:Heart disease is associated with re-expression of key transcription factors normally active only during prenatal development of the heart. However, the impact of this reactivation on the regulatory landscape in heart disease is unclear. Here, we use RNA-seq and ChIP-seq targeting a histone modification associated with active transcriptional enhancers to generate genome-wide enhancer maps from left ventricle tissue from up to 26 healthy controls, 18 individuals with idiopathic dilated cardiomyopathy (DCM), and five fetal hearts. Healthy individuals have a highly reproducible epigenomic landscape, consisting of more than 33,000 predicted heart enhancers. In contrast, we observe reproducible disease-associated changes in activity at 6,850 predicted heart enhancers. Combined analysis of adult and fetal samples reveals that the heart disease epigenome and transcriptome both acquire fetal-like characteristics, with 3,400 individual enhancers sharing fetal regulatory properties. We also provide a comprehensive data resource (http://heart.lbl.gov) for the mechanistic exploration of DCM etiology.

| S-EPMC9534044 | biostudies-literature

Genome-wide fetalization of enhancer architecture in heart disease

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

2019-04-02 | GSE126573 | GEO

Genome-wide landscape and functional necessity of heart enhancers

Project description:Analysis of the transcriptional changes in the heart resulting from the loss of cardiac enhancers. As there remains a limited understanding of the phenotypic consequences of enhancer mutations, we examined the impact of loss of function mutations by deleting two enhancers near heart disease genes in mice. In both cases, we observed loss of target gene expression, as well as cardiac phenotypes consistent with heart disease in humans, highlighting the functional importance of enhancers for normal heart function, as well as the potential contribution of enhancer mutations to heart disease. Hearts were dissected from wild-type and enhancer-null mice (either embryonic or adult) and processed for deep RNA-seq analysis.

2016-09-06 | E-GEOD-75907 | biostudies-arrayexpress

ChIP-seq Identification of Weakly Conserved Heart Enhancers

Project description:Accurate control of tissue-specific gene expression plays a pivotal role in heart development. However, few cardiac transcriptional enhancers have thus far been identified. Extreme non-coding sequence conservation successfully predicts enhancers active in many tissues, but fails to identify substantial numbers of enhancers active in the heart. We used ChIP-seq with the enhancer-associated protein p300 from mouse embryonic heart tissue to identify over three thousand candidate heart enhancers genome-wide. In contrast to other studied tissues at this time-point, most candidate heart enhancers are not deeply conserved in vertebrate evolution. Nevertheless, the testing of 130 candidate regions in a transgenic mouse assay revealed that most of them reproducibly function as enhancers active in the heart, irrespective of their degree of evolutionary constraint. These results provide evidence for tissue-dependent differences in evolutionary constraint of enhancers acting through the transcriptional co-activator p300 at this time-point, and identify a large population of poorly conserved heart enhancers. Examination of p300 binding in embryonic stage 11.5 mouse heart and midbrain

2010-08-22 | E-GEOD-22549 | biostudies-arrayexpress

An injury responsive enhancer promotes heart regeneration in zebrafish

Project description:we profiled chromatin accessibility of zebrafish endothelial cells after amputation injury and identify an mmp14b endothelial enhancer induced by heart injury in zebrafish. We show that the enhancer is required for mmp14b expression and regeneration in response to heart injury. Moreover, the enhancer depends on a consensus TEAD-binding motif, suggesting a role for Hippo signaling upstream of mmp14b.

2023-07-24 | GSE211424 | GEO

CTCF orchestrated enhancer hijacking accelerated tumorigenesis through remodeling 3D chromosomal architecture in NTS locus [ChIP-seq]

Project description:CTCF orchestrated enhancer hijacking accelerated tumorigenesis through remodeling 3D chromosomal architecture in NTS locus [ChIP-seq]

| PRJNA562261 | 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