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Links from GEO DataSets

Items: 20

1.

Coronary Artery Disease Associated Transcription Factor TCF21 Regulates Smooth Muscle Precursor Cells that Contribute to the Fibrous Cap

(Submitter supplied) Recent genome wide association studies have identified a number of genes that contribute to the risk for coronary heart disease. One such gene, TCF21, encodes a basic-helix-loop-helix transcription factor believed to serve a critical role in the development of epicardial progenitor cells that give rise to coronary artery smooth muscle cells (SMC) and cardiac fibroblasts. Using reporter gene and immunolocalization studies with mouse and human tissues we have found that vascular TCF21 expression in the adult is restricted primarily to adventitial cells associated with coronary arteries and also medial SMC in the proximal aorta of mouse. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: BED
2.

Coronary disease associated gene TCF21 inhibits smooth muscle cell differentiation by blocking the myocardin-serum response factor pathway

(Submitter supplied) Coronary disease associated gene TCF21 inhibits smooth muscle cell differentiation by blocking the myocardin-serum response factor pathway
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL9115 GPL16791
6 Samples
Download data: BED, BW
Series
Accession:
GSE124011
ID:
200124011
3.

Coronary artery disease genes SMAD3 and TCF21 promote opposing interactive genetic programs that regulate smooth muscle cell differentiation and disease risk

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Third-party reanalysis
Platforms:
GPL20301 GPL20795
8 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE115319
ID:
200115319
4.

Coronary artery disease genes SMAD3 and TCF21 promote opposing interactive genetic programs that regulate smooth muscle cell differentiation and disease risk [RNA-seq]

(Submitter supplied) Although numerous genetic loci have been associated with coronary artery disease (CAD) with genome wide association studies (GWAS), efforts are needed to identify the causal genes in these loci and link them into fundamental signaling pathways. Toward that end, experiments reported here extend our investigation of the disease mechanism of CAD associated gene SMAD3, a central transcriptional intermediate in the TGFb pathway, investigating its role in smooth muscle biology. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
6 Samples
Download data: TXT
5.

Coronary artery disease genes SMAD3 and TCF21 promote opposing interactive genetic programs that regulate smooth muscle cell differentiation and disease risk [ChIP-seq]

(Submitter supplied) Although numerous genetic loci have been associated with coronary artery disease (CAD) with genome wide association studies (GWAS), efforts are needed to identify the causal genes in these loci and link them into fundamental signaling pathways. Toward that end, experiments reported here extend our investigation of the disease mechanism of CAD associated gene SMAD3, a central transcriptional intermediate in the TGFb pathway, investigating its role in smooth muscle biology. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Third-party reanalysis
Platform:
GPL20795
2 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE115317
ID:
200115317
6.

Characterization of TCF21 downstream target regions identifies a transcriptional network linking multiple independent coronary artery disease loci

(Submitter supplied) Recent meta-analyses of genome wide association studies (GWAS) have identified approximately 150 loci that are associated with coronary artery disease (CAD). To link the causal genes in these loci to functional transcriptional networks, we have used chromatin immunoprecipitation sequencing (ChIP-Seq) with human coronary artery smooth muscle cells (HCASMC) to investigate the cellular and molecular program downstream of one CAD associated transcription factor, TCF21. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL9115
8 Samples
Download data: BED
Series
Accession:
GSE61369
ID:
200061369
7.

TCF21 and Aryl-hydrocarbon receptor gene cooperate to activate a pro-atherosclerotic gene expression program

(Submitter supplied) Genome-wide association studies (GWAS) for coronary artery disease (CAD, also termed coronary heart disease, CHD) have discovered and validated 48 loci genome-wide and recent 1000-Genomes based meta-analyses have discovered additional 8 loci with significant association, however, true follow-up studies on the mechanisms of association are still scarce. Here we analyze the relationship of two transcription factors, TCF21, one of the lead GWAS candidate genes for coronary artery disease and AHR, aryl hydrocarbon receptor, which previously was not implicated as fundamental for the atherosclerotic process. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: CSV, TXT
8.

Single cell analysis of smooth muscle cell phenotypic modulation in vivo during disease in mice and humans

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
31 Samples
Download data: BED
Series
Accession:
GSE131780
ID:
200131780
9.

Single cell analysis of smooth muscle cell phenotypic modulation in vivo during disease in mice and humans [pooled TCF21 ChIPseq]

(Submitter supplied) In response to various stimuli, vascular smooth muscle cells (SMCs) can de-differentiate, proliferate and migrate in a process known as phenotypic modulation. However, the phenotype of modulated SMCs in vivo during atherosclerosis and the influence of this process on coronary artery disease (CAD) risk have not been clearly established. Using single cell RNA sequencing, we comprehensively characterized the transcriptomic phenotype of modulated SMCs in vivo in atherosclerotic lesions of both mouse and human. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20795
1 Sample
Download data: BED
Series
Accession:
GSE131779
ID:
200131779
10.

Single cell analysis of smooth muscle cell phenotypic modulation in vivo during disease in mice and humans [human scRNA-seq]

(Submitter supplied) In response to various stimuli, vascular smooth muscle cells (SMCs) can de-differentiate, proliferate and migrate in a process known as phenotypic modulation. However, the phenotype of modulated SMCs in vivo during atherosclerosis and the influence of this process on coronary artery disease (CAD) risk have not been clearly established. Using single cell RNA sequencing, we comprehensively characterized the transcriptomic phenotype of modulated SMCs in vivo in atherosclerotic lesions of both mouse and human. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: TXT
Series
Accession:
GSE131778
ID:
200131778
11.

Single cell analysis of smooth muscle cell phenotypic modulation in vivo during disease in mice and humans [mouse CITE-seq]

(Submitter supplied) In response to various stimuli, vascular smooth muscle cells (SMCs) can de-differentiate, proliferate and migrate in a process known as phenotypic modulation. However, the phenotype of modulated SMCs in vivo during atherosclerosis and the influence of this process on coronary artery disease (CAD) risk have not been clearly established. Using single cell RNA sequencing, we comprehensively characterized the transcriptomic phenotype of modulated SMCs in vivo in atherosclerotic lesions of both mouse and human. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21626
4 Samples
Download data: TXT
Series
Accession:
GSE131777
ID:
200131777
12.

Single cell analysis of smooth muscle cell phenotypic modulation in vivo during disease in mice and humans [mouse scRNA-seq]

(Submitter supplied) In response to various stimuli, vascular smooth muscle cells (SMCs) can de-differentiate, proliferate and migrate in a process known as phenotypic modulation. However, the phenotype of modulated SMCs in vivo during atherosclerosis and the influence of this process on coronary artery disease (CAD) risk have not been clearly established. Using single cell RNA sequencing, we comprehensively characterized the transcriptomic phenotype of modulated SMCs in vivo in atherosclerotic lesions of both mouse and human. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
18 Samples
Download data: TXT
Series
Accession:
GSE131776
ID:
200131776
13.

Biobank of Karolinska Endarterectomy (BiKE)

(Submitter supplied) A biobank collection of carotid plaque samples taken from patients undergoing endarterectomy operations.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
223 Samples
Download data: CEL
Series
Accession:
GSE21545
ID:
200021545
14.

The environment-sensing aryl-hydrocarbon receptor inhibits the chondrogenic fate of modulated smooth muscle cells in atherosclerotic lesions

(Submitter supplied) Aryl-hydrocarbon receptor protects against endochondral ossification of modulated smooth muscle cells in atherosclerosis Introduction: Smooth muscle cells (SMC) play a critical role in atherosclerosis. The Aryl hydrocarbon receptor (AHR) is an environment-sensing transcription factor that contributes to vascular development, and has been implicated in coronary artery disease (CAD) risk. We hypothesized that AHR can affect atherosclerosis by regulating phenotypic modulation of SMC. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24676 GPL20301 GPL21103
34 Samples
Download data: BW, TXT
Series
Accession:
GSE150768
ID:
200150768
15.

TCF21 and AP-1 interact through epigenetic modifications to regulate coronary artery disease gene expression

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20795
12 Samples
Download data: BROADPEAK
Series
Accession:
GSE122758
ID:
200122758
16.

TCF21 and AP-1 interact through epigenetic modifications to regulate coronary artery disease gene expression [ChIP-Seq]

(Submitter supplied) The majority of genetic variation associated with coronary artery disease (CAD) resides in non- coding regions that are expected to involve transcriptional and epigenetic mechanisms of gene expression. We have identified a transcriptional network downstream of the CAD associated transcription factor (TF) TCF21 and provide evidence for TCF21 colocalization and co- regulation with the activator protein-1 (AP-1) complex in disease loci. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20795
6 Samples
Download data: BED, BROADPEAK
Series
Accession:
GSE122757
ID:
200122757
17.

TCF21 and AP-1 interact through epigenetic modifications to regulate coronary artery disease gene expression [ATAC-Seq]

(Submitter supplied) The majority of genetic variation associated with coronary artery disease (CAD) resides in non- coding regions that are expected to involve transcriptional and epigenetic mechanisms of gene expression. We have identified a transcriptional network downstream of the CAD associated transcription factor (TF) TCF21 and provide evidence for TCF21 colocalization and co- regulation with the activator protein-1 (AP-1) complex in disease loci. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20795
6 Samples
Download data: BED, BROADPEAK
Series
Accession:
GSE122756
ID:
200122756
18.

Quantitative trait loci mapped for TCF21 binding, chromatin accessibility and chromosomal looping in coronary artery smooth muscle cells reveal molecular mechanisms of coronary disease loci [array]

(Submitter supplied) To better understand the fundamental molecular mechanisms that contribute to complex human diseases such as coronary artery disease (CAD), we have created a catalog of genetic variants associated with three stages of transcriptional cis-regulation in primary human coronary artery vascular smooth muscle cells. To this end, we used a pooling approach to map quantitative trait locus associations (QTLs) for TCF21 binding (ChIPseq), chromatin accessibility (ATACseq), and chromosomal looping (HiC). more...
Organism:
Homo sapiens
Type:
SNP genotyping by SNP array; Genome variation profiling by SNP array
Platform:
GPL24127
15 Samples
Download data: TXT
Series
Accession:
GSE150403
ID:
200150403
19.

Quantitative trait loci mapped for TCF21 binding, chromatin accessibility and chromosomal looping in coronary artery smooth muscle cells reveal molecular mechanisms of coronary disease loci

(Submitter supplied) To better understand the fundamental molecular mechanisms that contribute to complex human diseases such as coronary artery disease (CAD), we have created a catalog of genetic variants associated with three stages of transcriptional cis-regulation in primary human coronary artery vascular smooth muscle cells. To this end, we used a pooling approach to map quantitative trait locus associations (QTLs) for TCF21 binding (ChIPseq), chromatin accessibility (ATACseq), and chromosomal looping (HiC). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other; SNP genotyping by SNP array; Genome variation profiling by SNP array
Platforms:
GPL20301 GPL24127 GPL20795
18 Samples
Download data: BED, BEDPE, HIC, TXT
Series
Accession:
GSE141752
ID:
200141752
20.

Quantitative trait loci mapped for TCF21 binding, chromatin accessibility and chromosomal looping in coronary artery smooth muscle cells reveal molecular mechanisms of coronary disease loci (ChIP-Seq)

(Submitter supplied) To better understand the fundamental molecular mechanisms that contribute to complex human diseases such as coronary artery disease (CAD), we have created a catalog of genetic variants associated with three stages of transcriptional cis-regulation in primary human coronary artery vascular smooth muscle cells. To this end, we used a pooling approach to map quantitative trait locus associations (QTLs) for TCF21 binding (ChIPseq), chromatin accessibility (ATACseq), and chromosomal looping (HiC). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20795
1 Sample
Download data: BED
Series
Accession:
GSE141751
ID:
200141751
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