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Links from GEO DataSets

Items: 20

1.

Histone 3 Lysine 9 Dimethylation Attenuates the Vascular Smooth Muscle Cell Inflammatory Response

(Submitter supplied) Vascular inflammation underlies cardiovascular disease. Vascular smooth muscle cells (VSMCs) upregulate selective genes, including matrix metalloproteinases (MMPs) and pro-inflammatory cytokines in response to local inflammation, which directly contribute to vascular disease and adverse clinical outcome. Identification of factors controlling VSMC responses to inflammation is therefore of considerable therapeutic importance. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
4 Samples
Download data: TXT
Series
Accession:
GSE131212
ID:
200131212
2.

BACH1 Deficiency Prevents Neointima Formation and Maintains the Differentiated Phenotype of Vascular Smooth Muscle Cell by Regulating Chromatin Accessibility

(Submitter supplied) Chromatin accessibility is important for cell fate determination in differentiation and multiple pathophysiological processes. Here, we report a transcription factor BACH1, facilitates the recruitment of G9a and YAP, maintains the state of H3K9me2 and decreases the chromatin accessibility at the promoter of VSMC marker genes, thereby repressing their expression and contributing to dedifferentiated VSMC phenotype. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
20 Samples
Download data: BW, FPKM_TRACKING
3.

The genomic distribution and gene expression profiling of cardiomyocyte-enriched populations

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL19057 GPL17021 GPL6887
42 Samples
Download data: BW, IDAT
Series
Accession:
GSE93754
ID:
200093754
4.

Gene expression profiling of cardiomyocyte-enriched populations isolated from G9a-KO and Cre mice

(Submitter supplied) The role of the histone mehyltrasferase G9a (also known as Ehmt2) in heart has not been extensively studied. To identify the genes regulated by G9a in the normal heart, we first generated a conditional, cardiac-specific KO mouse for this gene using the Cre-Lox approach, crossing G9a flox/flox mice with αMHC-MerCreMer mice (Cre mice were used as controls). Then, we sequenced total RNA (Total-RNA-seq) from cardiomyocyte-enriched populations isolated from G9a-KO and Cre mice, and compared the two expression profiles.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
4 Samples
Download data: BW
Series
Accession:
GSE93753
ID:
200093753
5.

The genomic distribution of G9a, H3K9me2 and H3K27me3 in cardiac hypertrophy.

(Submitter supplied) The role of the histone methyltrasferase G9a (also known as Ehmt2) in the normal heart has not been studied extensively. To identify which genes were direct targets of G9a in hypertrophic cardiomyocytes, we performed ChIP-seq for G9a and H3K9me2 – the main histone methylation catalysed by the HMT – on cardiomyocytes isolated from normal mice (sham) and mice subject to transverse aortic constriction (TAC) for 1 wk, a surgical procedure that causes cardiac hypertrophy following the induction of pressure overload. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
14 Samples
Download data: BED, BW
Series
Accession:
GSE93752
ID:
200093752
6.

Gene expression profiling of cardiomyocyte-enriched populations isolated from mice subject to transverse aortic constriction (TAC) and treated with BIX-01294 for 1 week

(Submitter supplied) The role of the histone mehyltrasferase G9a (also known as Ehmt2) in cardiac hypertrophy has not been studied extensively. To address how G9a promotes cardiac hypertrophy, we assessed the gene expression signature defined by G9a in cardiomyocytes (CM) of mice subject to transverse aortic constriction (TAC) for 1 wk, a surgical procedure that causes cardiac hypertrophy following the induction of pressure overload. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
6 Samples
Download data: IDAT, TXT
Series
Accession:
GSE93691
ID:
200093691
7.

The genomic distribution of G9a, H3K9me2, H3K27me3 and Mef2c in cardiomyocyte-enriched populations isolated from G9a-KO and Cre mice

(Submitter supplied) The role of the histone methyltrasferase G9a (also known as Ehmt2) in the normal heart has not been studied extensively. To identify the genomic regions bound to G9a in cardiomyocytes (CMs),we first generated a conditional, cardiac-specific KO mouse for this gene using the Cre-Lox approach, crossing G9a flox/flox mice with αMHC-MerCreMer mice (Cre mice were used as controls). Then we performed ChIP-seq for G9a and H3K9me2 – the main histone methylation catalysed by the HMT – on isolated G9a-KO and Cre CMs, and considered the best G9a-bound genomic regions as those that had a loss or decrease of G9a binding as well as a lower level of H3K9me2 in G9a-KO CMs. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
18 Samples
Download data: BED, BW
Series
Accession:
GSE93690
ID:
200093690
8.

Regulation of 3D genome organization, transcription and histone H3K9me2 by histone H3K9 methyltransferases

(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
Platform:
GPL21273
56 Samples
Download data: BW, TXT
Series
Accession:
GSE169106
ID:
200169106
9.

Regulation of 3D genome organization, transcription and histone H3K9me2 by histone H3K9 methyltransferases [HiC]

(Submitter supplied) Histone H3 lysine 9 dimethylation (H3K9me2) is a highly conserved silencing epigenetic mark. Chromatin marked with H3K9me2 forms large domains in mammalian cells and overlaps well with lamina-associated domains and the B compartment defined by Hi-C. However, the role of H3K9me2 in 3-dimensional (3D) genome organization remains unclear. We investigated genome-wide H3K9me2 distribution, transcriptome, and 3D genome organization in mouse embryonic stem cells following the inhibition or depletion of five H3K9 methyltransferases (MTases): G9a, GLP, SETDB1, SUV39H1, and SUV39H2. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL21273
8 Samples
Download data: TXT
Series
Accession:
GSE169103
ID:
200169103
10.

Regulation of 3D genome organization, transcription and histone H3K9me2 by histone H3K9 methyltransferases [ChIP-Seq]

(Submitter supplied) Histone H3 lysine 9 dimethylation (H3K9me2) is a highly conserved silencing epigenetic mark. Chromatin marked with H3K9me2 forms large domains in mammalian cells and overlaps well with lamina-associated domains and the B compartment defined by Hi-C. However, the role of H3K9me2 in 3-dimensional (3D) genome organization remains unclear. We investigated genome-wide H3K9me2 distribution, transcriptome, and 3D genome organization in mouse embryonic stem cells following the inhibition or depletion of five H3K9 methyltransferases (MTases): G9a, GLP, SETDB1, SUV39H1, and SUV39H2. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21273
40 Samples
Download data: BW
Series
Accession:
GSE169099
ID:
200169099
11.

Regulation of 3D genome organization, transcription and histone H3K9me2 by histone H3K9 methyltransferases [RNA-Seq]

(Submitter supplied) Histone H3 lysine 9 dimethylation (H3K9me2) is a highly conserved silencing epigenetic mark. Chromatin marked with H3K9me2 forms large domains in mammalian cells and overlaps well with lamina-associated domains and the B compartment defined by Hi-C. However, the role of H3K9me2 in 3-dimensional (3D) genome organization remains unclear. We investigated genome-wide H3K9me2 distribution, transcriptome, and 3D genome organization in mouse embryonic stem cells following the inhibition or depletion of five H3K9 methyltransferases (MTases): G9a, GLP, SETDB1, SUV39H1, and SUV39H2. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21273
8 Samples
Download data: TXT
Series
Accession:
GSE169098
ID:
200169098
12.

Histone H3K9 Methyltransferase G9a Represses PPARγ Expression and Adipogenesis

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL1261 GPL13112
12 Samples
Download data: BED, CEL
Series
Accession:
GSE41457
ID:
200041457
13.

Histone H3K9 Methyltransferase G9a Represses PPARγ Expression and Adipogenesis [Affymetrix expression data]

(Submitter supplied) PPARγ promotes adipogenesis while Wnt proteins inhibit adipogenesis. However, the mechanisms that control expression of these positive and negative master regulators of adipogenesis remain incompletely understood. By genome-wide histone methylation profiling in preadipocytes, we find that among gene loci encoding adipogenesis regulators, histone methyltransferase (HMT) G9a-mediated repressive epigenetic mark H3K9me2 is enriched on the entire PPARγ locus. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
4 Samples
Download data: CEL
Series
Accession:
GSE41456
ID:
200041456
14.

Histone H3K9 Methyltransferase G9a Represses PPARγ Expression and Adipogenesis [ChIP-Seq and RNA-Seq data]

(Submitter supplied) PPARγ promotes adipogenesis while Wnt proteins inhibit adipogenesis. However, the mechanisms that control expression of these positive and negative master regulators of adipogenesis remain incompletely understood. By genome-wide histone methylation profiling in preadipocytes, we find that among gene loci encoding adipogenesis regulators, histone methyltransferase (HMT) G9a-mediated repressive epigenetic mark H3K9me2 is enriched on the entire PPARγ locus. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: BED
Series
Accession:
GSE41455
ID:
200041455
15.

BAF60a Deficiency in Vascular Smooth Muscle Cells Prevents Abdominal Aortic Aneurysm Formation by Attenuating Vascular Inflammation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL20301
24 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE153449
ID:
200153449
16.

Transciptomic analysis of human aortic smooth muscle cells (HASMCs) with BAF60a knockdown

(Submitter supplied) We used NGS-derived transcriptome profiling (RNA-seq) to compare the transcriptional difference between human aortic smooth muscle cells (HASMCs) transfected with 30nM siRNA targeting BAF60a (siBAF60a) or non-targeting siRNA (siControl)
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: TXT
17.

Transciptomic analysis of human aortic smooth muscle cells (HASMCs) with BAF60a overexpression

(Submitter supplied) We used NGS-derived transcriptome profiling (RNA-seq) to compare the transcriptional difference between human aortic smooth muscle cells (HASMCs) infected with 20MOI adenovirus encoding human BAF60a (AdBAF60a) or GFP (AdGFP)
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: TXT
18.

Genome-wide maps of chromatin state changes in BAF60a deficient human aortic smooth muscle cells (HASMCs)

(Submitter supplied) We compared BRG1 binding and histone modification states between siControl and siBAF60a transfected human aortic smooth muscle cells (HASMCs) through ChIP sequencing.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
10 Samples
Download data: BIGWIG
Series
Accession:
GSE153446
ID:
200153446
19.

UHRF1-mediated epigenetic regulation of smooth muscle cell modulates development of vascular pathologies

(Submitter supplied) Adult vascular smooth muscle cells (VSMCs) dedifferentiate in response to extracellular cues such as vascular damage and inflammation. Dedifferentiated VSMCs are proliferative, migratory, less contractile, and can contribute to vascular repair as well as to cardiovascular pathologies such as intimal hyperplasia/restenosis in coronary artery and arterial aneurysm. We here demonstrate the role of ubiquitin-like containing PHD and RING finger domains 1 (UHRF1) as an epigenetic master regulator of VSMC plasticity. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
8 Samples
Download data: IDAT, TXT
Series
Accession:
GSE99472
ID:
200099472
20.

Chromatin dynamics and the role of G9a in gene regulation and enhancer silencing during early mouse development

(Submitter supplied) Early mouse development is accompanied by dynamic changes in chromatin modifications, including G9a-mediated histone H3 lysine 9 dimethylation (H3K9me2), which is essential for embryogenesis. Here we show that H3K9me2 directs repression of 2-cell stage specific genes in nascent embryos to facilitate preimplantation development. Thereafter, genome-wide accumulation of H3K9me2 is crucial for postimplantation development, and coincides with redistribution of EZH2-dependent histone H3 lysine 27 trimethylation (H3K27me3). more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL18480 GPL13112 GPL17021
59 Samples
Download data: BEDGRAPH, TXT
Series
Accession:
GSE70355
ID:
200070355
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