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Items: 20

1.

Temporal Analyses of Cardiac Chromatin Accessibility, DNA Methylation and Epigenomic Structure Reveal Locus-Specific Regulation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL21493 GPL19057 GPL24247
47 Samples
Download data: BW, CGMAP, TAR
Series
Accession:
GSE154521
ID:
200154521
2.

Temporal Analyses of Cardiac Chromatin Accessibility, DNA Methylation and Epigenomic Structure Reveal Locus-Specific Regulation [RRBS]

(Submitter supplied) Heart failure can be induced or ameliorated by regulation of chromatin modifying enzymes. Because so many chromatin factors regulate gene expression, we used ATAC-seq to report the status of a given locus at any time—the sum total of all epigenetic modifiers—in a mouse model of pressure overload hypertrophy. Early compensation of pressure overload at 3 days was associated with widespread changes in chromatin accessibility and DNA methylation, the majority of which persisted to the decompensated phase (3 weeks), revealing the temporal nature of epigenomic compensation to pathologic stimuli. more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platforms:
GPL24247 GPL21493
23 Samples
Download data: CGMAP
Series
Accession:
GSE154520
ID:
200154520
3.

Temporal Analyses of Cardiac Chromatin Accessibility, DNA Methylation and Epigenomic Structure Reveal Locus-Specific Regulation [RNA-seq]

(Submitter supplied) Heart failure can be induced or ameliorated by regulation of chromatin modifying enzymes. Because so many chromatin factors regulate gene expression, we used ATAC-seq to report the status of a given locus at any time—the sum total of all epigenetic modifiers—in a mouse model of pressure overload hypertrophy. Early compensation of pressure overload at 3 days was associated with widespread changes in chromatin accessibility and DNA methylation, the majority of which persisted to the decompensated phase (3 weeks), revealing the temporal nature of epigenomic compensation to pathologic stimuli. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: TAR
Series
Accession:
GSE154519
ID:
200154519
4.

Temporal Analyses of Cardiac Chromatin Accessibility, DNA Methylation and Epigenomic Structure Reveal Locus-Specific Regulation [ATAC-seq]

(Submitter supplied) Heart failure can be induced or ameliorated by regulation of chromatin modifying enzymes. Because so many chromatin factors regulate gene expression, we used ATAC-seq to report the status of a given locus at any time—the sum total of all epigenetic modifiers—in a mouse model of pressure overload hypertrophy. Early compensation of pressure overload at 3 days was associated with widespread changes in chromatin accessibility and DNA methylation, the majority of which persisted to the decompensated phase (3 weeks), revealing the temporal nature of epigenomic compensation to pathologic stimuli. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
12 Samples
Download data: BW
Series
Accession:
GSE154518
ID:
200154518
5.

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

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platforms:
GPL13112 GPL21103
17 Samples
Download data: GTF, HIC, NARROWPEAK
Series
Accession:
GSE96693
ID:
200096693
6.

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

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL21103
3 Samples
Download data: HIC
Series
Accession:
GSE96692
ID:
200096692
7.

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

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: NARROWPEAK
Series
Accession:
GSE96691
ID:
200096691
8.

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

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
10 Samples
Download data: GTF
Series
Accession:
GSE96690
ID:
200096690
9.

Disruption of cardiac Med1 inhibits RNA polymerase-II promoter occupancy and induces chromatin remodeling

(Submitter supplied) The Mediator co-activator complex directs gene specific expression by binding distal enhancer-bound transcription factors through its Med1 subunit while bridging to RNA Polymerase-II (Pol-II) at gene promoters. In addition, Mediator scaffolds epigenetic modifying enzymes that determine local DNA accessibility. We previously found that deletion of Med1 in cardiomyocytes deregulates more than 5000 genes and promotes acute heart failure and hypothesize Med1 deficiency disrupts enhancer-promoter coupling. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18480
7 Samples
Download data: BW
Series
Accession:
GSE118965
ID:
200118965
10.

Genome-wide chromatin state in non-failing and dilated cardiomyaphty human left ventricles

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
30 Samples
Download data
Series
Accession:
GSE135956
ID:
200135956
11.

Genome-wide chromatin state in non-failing and dilated cardiomyaphty human left ventricles [PLAC-seq]

(Submitter supplied) We conducted chromatin immunoprecipitation followed by sequencing (ChIP-seq) and proximity ligation-assisted ChIP-seq (PLAC-seq) for enhancers and promoters (E-P) using left ventricular tissues from dilated cardiomyopathy (DCM) patients and non-heart failure (NF) donors. Differential active enhancer H3K27ac and promoter H3K4me3 regions were identified between NF and DCM. While the average read density (ARD) for H3K27ac is similar between NF and DCM, the ARD of H3K4me3 is significantly lower in DCM samples than in NF.Super-enhancer (SE) analysis revealed that 929 and 129 genes linked to NF- and DCM-specific SE, respectively, and three unique SE-associated genes between NF and DCM were identified.Moreover, the differential E-P interactions were observed in the known heart failure gene loci and are correlated with the gene expression levels. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: HIC
Series
Accession:
GSE135954
ID:
200135954
12.

Genome-wide chromatin state in non-failing and dilated cardiomyaphty human left ventricles [ChIP-Seq]

(Submitter supplied) We conducted chromatin immunoprecipitation followed by sequencing (ChIP-seq) and proximity ligation-assisted ChIP-seq (PLAC-seq) for enhancers and promoters (E-P) using left ventricular tissues from dilated cardiomyopathy (DCM) patients and non-heart failure (NF) donors. Differential active enhancer H3K27ac and promoter H3K4me3 regions were identified between NF and DCM. While the average read density (ARD) for H3K27ac is similar between NF and DCM, the ARD of H3K4me3 is significantly lower in DCM samples than in NF.Super-enhancer (SE) analysis revealed that 929 and 129 genes linked to NF- and DCM-specific SE, respectively, and three unique SE-associated genes between NF and DCM were identified.Moreover, the differential E-P interactions were observed in the known heart failure gene loci and are correlated with the gene expression levels. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
22 Samples
Download data: BED
Series
Accession:
GSE135953
ID:
200135953
13.

Cell Type-Specific Chromatin Signatures Underline Regulatory DNA Elements in Human Induced Pluripotent Stem Cells and Somatic Cells

(Submitter supplied) Regulatory DNA elements in the human genome play important roles in determining the transcriptional abundance and spatiotemporal gene expression. It is a mystery how chromatin marks in regulatory elements are modulated to establish cell type-specific gene expression. Here we profiled a variety of epigenetic marks in the regulatory elements using massive ChIP-seq (n=84). We uncovered two classes of regulatory elements: Class I was identified with ubiquitous enhancer (H3K4me1) and promoter (H3K4me3) marks in all cell types, whereas Class II was enriched with H3K4me1 and H3K4me3 in a cell type-specific manner. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL16791
96 Samples
Download data: TXT
14.

BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Rattus norvegicus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
60 Samples
Download data: CEL, WIG
Series
Accession:
GSE48112
ID:
200048112
15.

BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure [NRVM Expression]

(Submitter supplied) Heart failure (HF) is driven via interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. While pathologic gene transactivation in this context is known to be associated with recruitment of histone acetyl-transferases and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. We therefore undertook a first study of acetyl-lysine reader proteins, or bromodomains, in HF. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platform:
GPL1355
20 Samples
Download data: CEL
Series
Accession:
GSE48111
ID:
200048111
16.

BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure [Mouse Heart Expression]

(Submitter supplied) Heart failure (HF) is driven via interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. While pathologic gene transactivation in this context is known to be associated with recruitment of histone acetyl-transferases and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. We therefore undertook a first study of acetyl-lysine reader proteins, or bromodomains, in HF. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
27 Samples
Download data: CEL
Series
Accession:
GSE48110
ID:
200048110
17.

BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure [ChIP-Seq]

(Submitter supplied) Heart failure is driven by the interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. Coordinate activation of developmental, inflammatory, fibrotic and growth regulators underlies the hallmark phenotypes of pathologic cardiac hypertrophy and contractile failure. While transactivation in this context is known to be associated with recruitment of histone acetyl-transferase enzymes and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL13112 GPL9250
13 Samples
Download data: WIG
Series
Accession:
GSE46668
ID:
200046668
18.

Regulation of mouse chamber selective enhancers

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; synthetic construct
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other; Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL26526 GPL24247
82 Samples
Download data: BW, TXT
Series
Accession:
GSE215065
ID:
200215065
19.

Chamber selective enhancers identified in vivo by AAV-MPRA

(Submitter supplied) Measurement the activity of candidate CSEs in aCMs and vCMs.
Organism:
synthetic construct; Mus musculus
Type:
Other
Platforms:
GPL26526 GPL24247
15 Samples
Download data: TXT
Series
Accession:
GSE215033
ID:
200215033
20.

Dense, systematic mutagenesis to identify the features required for CSEs

(Submitter supplied) Investigate the sequence features required for CSE activity and selectivity.
Organism:
synthetic construct; Mus musculus
Type:
Other
Platforms:
GPL26526 GPL24247
14 Samples
Download data: TXT
Series
Accession:
GSE215032
ID:
200215032
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