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Links from GEO DataSets

Items: 16

1.

Tead1 is required to maintain adult cardiomyocyte function

(Submitter supplied) Since Tead1 binds to MCAT promoter elements to regulate many muscle-specific genes, we performed a global transcriptome analysis in Tead1-deleted adult mouse hearts to assess Tead1 regulated pathways critical to CM function.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL13912
6 Samples
Download data: TXT
Series
Accession:
GSE85038
ID:
200085038
2.

Med1 Deletion in Heart Causes Dilated Cardiomyopathy

(Submitter supplied) Global gene expression analysis reveals that Med1 regulates many genes involved in energy metabolism, calcium signaling, and oxidative phosphorylation in myocardium.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
2 Samples
Download data: TXT
Series
Accession:
GSE65873
ID:
200065873
3.

Expression data from patient iPSC and iPSC-derived cardiomyocytes

(Submitter supplied) Dilated cardiomyopathy (DCM) is the leading cause of heart failure and transplantation worldwide. We used iPSCs to model this disease and compared gene expression change before and after gene therapy of cardiomyocytes derived from DCM-specific iPSCs. We used microarrays to detail the global gene expression of patient specific iPSCs, iPSC-derived cardiomyocytes and its response to gene therapy.
Organism:
Homo sapiens
Type:
Expression profiling by array
Datasets:
GDS4312 GDS4435
Platform:
GPL6244
17 Samples
Download data: CEL
Series
Accession:
GSE35108
ID:
200035108
4.
Full record GDS4435

Serca2a effect on Dilated Cardiomyopathy iPSC-derived cardiomyocytes

Analysis of DCM iPSC-derived cardiomyocytes treated with sarcoplasmic reticulum Ca2+ adenosine triphosphatase (Serca2a). Serca2a treatment improved the function of these cardiomyocytes. Results provide insight into the molecular basis of Serca2a-mediated repair of DCM iPSC-derived cardiomyocytes.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 cell type, 2 protocol sets
Platform:
GPL6244
Series:
GSE35108
8 Samples
Download data: CEL
5.
Full record GDS4312

Inherited dilated cardiomyopathy patient-specific induced pluripotent stem cells

Analysis of iPSCs derived from skin fibroblasts of Dilated Cardiomyopathy (DCM) family members carrying point mutation R173W in the sarcomeric protein cardiac troponin T (TNNT2) gene. Results provide insight into the molecular mechanisms underlying familial dilated cardiomyopathy.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 3 cell type, 2 genotype/variation, 9 individual sets
Platform:
GPL6244
Series:
GSE35108
9 Samples
Download data: CEL
6.

Expression Data from E16.5 hearts from WT and FOG-2R3K5A siblings

(Submitter supplied) Heart development is modulated by FOG-2/NuRD interactions. FOG-2R3K5A is unable to recuit the NuRD complex and this results in cardiac defects such as ASD, VSD, and thin ventricular walls We used microarrays to detail the changes in gene expression in FOG-2R3K5A hearts to determine misexpression of genes that may be causing the observed phenotypes.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE50426
ID:
200050426
7.

Znhit1-deficiency caused sarcoplasmic reticulum originated vacuolar cardiomyopathy

(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
Platform:
GPL24247
21 Samples
Download data: TXT
Series
Accession:
GSE194164
ID:
200194164
8.

CUT&Tag for H2A.Z using mouse heart tissues from control and Znhit1-deficient mice

(Submitter supplied) Znhit1 is an important subunit of the SRCAP complex, which regulates gene transcription by replacing histone H2A with a variant H2A.Z at gene promoter regions. Deletion of Znhit1 has also been reported to impact the incorporation of H2A.Z in genome. To explore the function of Znhit1 in heart tissues, we performed CUT&Tag assays for H2A.Z to examine the distribution changes of H2A.Z on the genome.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
9 Samples
Download data: TXT
Series
Accession:
GSE194162
ID:
200194162
9.

RNA-Seq for control and Znhit1-deficient heart tissues from postnatal day 17 and 25 mice

(Submitter supplied) To investigate the function of Znhit1 in mouse hearts, we deleted Znhit1 using conditional Znhit1-knockout mice (Znhit1 flox/flox; Myh6-Cre; Znhit1 cKO). Through RNA-Seq, we tested the genome-wide transcriptional changes at postnatal day 17 and 25.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: TXT
Series
Accession:
GSE194115
ID:
200194115
10.

R14del RNA-seq

(Submitter supplied) Arrhythmogenic cardiomyopathy (ACM) is characterized by life-threatening ventricular arrhythmias and sudden cardiac death and affects hundreds of thousands of patients worldwide. The deletion of Arginine 14 (p.R14del) in the phospholamban (PLN) gene has been implicated in the pathogenesis of ACM. PLN is a key regulator of sarcoplasmic reticulum (SR) Ca2+ cycling and cardiac contractility. Despite global gene and protein expression studies, the molecular mechanisms of PLN-R14del ACM pathogenesis remain unclear. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Other
Platform:
GPL24676
6 Samples
Download data: TAB
Series
Accession:
GSE217921
ID:
200217921
11.

Impaired Right Ventricular Calcium Cycling Is an Early Risk 2 Factor in R14del-Phospholamban Arrhythmias 

(Submitter supplied) We utilized humanized wild-type and R14 deletion (R14del) phospholamban (PLN) knock-in mice to determine the role of the inherited PLN-R14del on malignant right ventricular arrhythmias.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: TXT
Series
Accession:
GSE173684
ID:
200173684
12.

Tead1 regulation of β-cells II

(Submitter supplied) Purpose: The goal of this study is to determine the regulatory role of Tead1 in β-cells by analyzing the Tead1 cistrome and open chromatin in β-cells Methods: Isolated islets from WT C57bl6 mice of 12 weeks of age were flash frozen. For Chip-seq they were fixed with formaldehyde and then after sonication, IP was performed with Anti-Tead1 antibody or the IgG isotype control. For ATAC-seq 100,000 of the frozen nuclei were tagmented. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: BW
Series
Accession:
GSE157513
ID:
200157513
13.

Expression data from Tead1 beta cell KO

(Submitter supplied) Tead1 is a transcription factor downstream of the hippo pathway. Gene expression is compared between whole islets from beta cell specific tead1 KO (using Rip-Cre) and Floxed control islets
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE139228
ID:
200139228
14.

Tead1 regulation of β-cells

(Submitter supplied) Purpose: The goal of this study is to determine the regulatory role of tead1 in β-cells by analyzing the transcriptomal changes with Tead1 deletion in β-cells Methods: Isolated islet mRNA profiles of β-cell Tead1 KO mice compared to control floxed mice at 1 year of age were assessed by RNA-seq using Illumina Hiseq2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level using the CLC genomic workbench. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: XLSX
Series
Accession:
GSE139152
ID:
200139152
15.

Transcriptomic analyses of cardiomyopathy development in mice carrying the phospholamban p.(Arg14del) pathogenic variant, and comparison with ischemic heart disease

(Submitter supplied) Background: The p.(Arg14del) pathogenic variant (R14del) of the phospholamban (PLN) gene is a prevalent cause of cardiomyopathy with heart failure. The exact underlying pathophysiology is unknown, and a suitable therapy is unavailable. We aim to identify molecular perturbations underlying this cardiomyopathy in a clinically relevant PLN-R14del mouse model. Methods: We investigated progression of cardiomyopathy in PLN-R14∆/∆ mice using echocardiography, electrocardiography and histological tissue analysis. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
39 Samples
Download data: TXT
Series
Accession:
GSE168610
ID:
200168610
16.

TEAD1 and TEAD3 play redundant roles in human epidermal proliferation

(Submitter supplied) TEAD1 is critical in maintaining human epidermis proliferation. It may function through its enhancer function.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
3 Samples
Download data: BED
Series
Accession:
GSE138727
ID:
200138727
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