Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure

ABSTRACT: Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure

PROVIDER: PRJNA379857 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5349550_1.fastq.gz	Fastqsanger.gz
	SRR5349550_2.fastq.gz	Fastqsanger.gz
	SRR5349560.fastq.gz	Fastqsanger.gz
	SRR5349551_1.fastq.gz	Fastqsanger.gz
	SRR5349551_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 30

Similar Datasets

Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [HiC-seq]

Project description:Understanding the principles of endogenous chromatin structure has key implications for epigenetic therapy. To determine the mechanisms of genome structure-function in post-mitotic cells, genome-wide chromatin conformation capture was performed in cardiac myocytes, a non-dividing, differentiated cell responsible for cardiac contraction. Cardiac-specific CTCF knockout mice demonstrated that loss of CTCF had minimal effect on topologically associating domains; however, it selectively altered boundary strength and A/B compartmentalization, with gene expression changes mimicking those in heart failure. Loss of CTCF (or subjecting wild-type mice to clinically relevant pressure overload stress) remodeled long-range chromatin looping to alter 3D proximity of enhancers and disease causing genes. Depletion of CTCF was sufficient to induce heart failure in mice and human heart failure patients receiving mechanical unloading to attenuate disease progression show increased CTCF expression. These findings establish CTCF in the maintenance of chromatin looping and identify global chromatin remodeling as a causative factor in heart failure.

2017-08-30 | GSE96692 | GEO

Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [ChIP-seq]

2017-08-30 | GSE96691 | GEO

Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [RNA-seq]

2017-08-30 | GSE96690 | GEO

Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure

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

2017-08-30 | GSE96693 | GEO

Genome-wide mapping of CTCF binding in asynchronous and mitotic cells

Project description:CCCTC-binding factor (CTCF), a conserved and essential regulator of genome architecture bearing a unique complement of 11 zinc fingers (ZFs), has been reported to remain associated with chromatin throughout mitosis and has thus been proposed to act as a bookmark to ensure rapid reestablishment of chromatin structure after cell division. However, little is known about how CTCF is regulated during mitosis. Using a phospho-specific antibody, we found that phosphorylation of CTCF threonine 431, contained within an atypical ZF linker unique to vertebrate CTCF, is highly enriched in mitotic cells and that this phosphorylated form of CTCF is preferentially localized to mitotic chromosomes. We show that T431 mutations abolish the association of CTCF with mitotic chromatin, arguing that T431 phosphorylation is necessary for CTCF mitotic retention. Furthermore, mutation of the CTCF paralog BORIS to accommodate phosphorylation at the residue corresponding to CTCF T431 induces mitotic retention of BORIS. Our data support previous work demonstrating mitotic retention of CTCF and provide new insight into how CTCF remains associated with chromatin during mitosis. Furthermore, our results indicate that phosphorylation of ZF linkers is not exclusively associated with dissociation of ZF-containing proteins from DNA during mitosis.

2019-12-31 | GSE102019 | GEO

Mitotic bookmarking by CTCF and fast post-mitotic gene reactivation in ES cells

Project description:Mitotic bookmarking by CTCF and fast post-mitotic gene reactivation in ES cells

| PRJNA807661 | ENA

Mus musculus

Project description:Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [HiC-seq]

| PRJNA379860 | ENA

Mus musculus

Project description:Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [RNA-seq]

| PRJNA379887 | ENA

Mus musculus

Project description:Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [ChIP-seq]

| PRJNA379888 | ENA

Mapping of CTCF occupancy in interphase and mitosis cells

Project description:To address whether CTCF is involved in the transcription of early G1 genes immediately after mitotic exit, we carried out ChIP sequencing (ChIP-seq) experiments to evaluate CTCF binding to genomic DNA in asynchronous cells and nocodazole-arrested mitotic cells. Of the 62,996 peaks identified in the asynchronous cells, 41,397 peaks (65.71%) were lost in the mitotic cells. However, the 21,599 peaks (34.29%) were identified in the both conditions, indicating that the enrichment level of CTCF is decreased in the mitotic cells. It has been reported that expression profiles of the first 2 hours of G1 phase in HeLa cells. A scatter plot comparison of the genes expressed in the early G1 phase indicated the reduced CTCF binding level in the mitotic phase. These results indicate that CTCF was dissociated or CTCF bound to chromosomes was reduced in the mitotic chromatin and then may be re-associated to chromatin in the early G1 phase.

2019-06-18 | GSE83579 | 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