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Links from GEO DataSets

Items: 20

1.

Characterization of the effect of overexpressing the Nrg-1 (neuregulin-1) gene, using the cardiac driver line Nkx2.5-Cre, in E (embryonic day) 15.5 heart venticles

(Submitter supplied) To investigate the role of Nrg-1 in heart ventricular chamber development, we overexpressed Nrg-1 in cardiac lineages, harvested ventricles at E15.5, and determined gene expression profiles, using RNA-seq.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
8 Samples
Download data: TXT
Series
Accession:
GSE216467
ID:
200216467
2.

Role of Nrg-1 in the development of heart ventricular chamber in mice.

(Submitter supplied) To investigate the role of Nrg-1 in heart ventricular chamber development, we have used RNA-Seq to characterize the effect of Nrg-1 inactivation or over-expression in mouse embryos at E9.5 and E15.5. This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL17021 GPL21103
24 Samples
Download data
Series
Accession:
GSE216471
ID:
200216471
3.

Characterization of the effect of deleting the Nrg-1(neuregulin-1) gene, using the endothelial driver line Tie2-Cre in E (embryonic day) 9.5 hearts

(Submitter supplied) To investigate the role of Nrg-1 in heart ventricular chamber development we deleted Nrg-1 in endothelial lineages, harvested hearts at E9.5, and determined gene expression profiles, using RNA-seq.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: TXT
Series
Accession:
GSE216470
ID:
200216470
4.

Characterization of the effect of deleting the Nrg-1(neuregulin-1) gene, using the tamoxifen-inducible endothelial driver line Cdh5-CreERT in E (embryonic day) 15.5 hearts

(Submitter supplied) To investigate the role of Nrg-1 in heart ventricular chamber development, we induced a conditional Nrg-1 deletion in endothelial cells at E15.5, with tamoxifen, and determined gene expression profiles, using RNA-seq.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: TXT
Series
Accession:
GSE216469
ID:
200216469
5.

PRDM16 Is a Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle

(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
Platforms:
GPL24247 GPL21103
44 Samples
Download data: SF, TAR, TIFF
Series
Accession:
GSE179393
ID:
200179393
6.

PRDM16 Functions as A Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle (Spatial Transcriptomics)

(Submitter supplied) The loss of compact myocardial cardiomyocyte (compact CM) identity suggests that PRDM16 deficiency may dramatically alter the cellular composition in left ventricular (LV) compact myocardium. To test this hypothesis, we performed single-cell RNA-seq (scRNA-seq) to examine gene dysreulation in Prdm16cKO heart. We also performed Visium Spatial Transcriptomics (ST) to facilitate mapping CM clusters to their original locations in the heart. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: TAR, TIFF
Series
Accession:
GSE179392
ID:
200179392
7.

PRDM16 Functions as A Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle (scRNA-seq)

(Submitter supplied) The loss of compact myocardial cardiomyocyte (compact CM) identity suggests that PRDM16 deficiency may dramatically alter the cellular composition in left ventricular (LV) compact myocardium. To test this hypothesis, we performed single-cell RNA-seq (scRNA-seq) to examine gene dysreulation in Prdm16cKO heart. We also performed Visium Spatial Transcriptomics (ST) to facilitate mapping CM clusters to their original locations in the heart. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: TAR
Series
Accession:
GSE179390
ID:
200179390
8.

PRDM16 Functions as A Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle (bulk RNA-seq)

(Submitter supplied) Gene expression profiling in whole heart, left ventricle (LV) and right ventricle (RV) of WT and Prdm16 conditional knockout (Prdm16cKO) mouse (Prdm16flox/flox; Xmlc2-Cre) at embryonic day 13.5 (E13.5).
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
22 Samples
Download data: SF
Series
Accession:
GSE179386
ID:
200179386
9.

PRDM16 Functions as A Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle (ChIP-seq)

(Submitter supplied) Identification of genome-wide PRDM16 binding sites in E13.5 whole mouse heart, as well as in isolated left ventricle (LV) and right ventricle (RV).
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21103
14 Samples
Download data: BED, NARROWPEAK
Series
Accession:
GSE179371
ID:
200179371
10.

The Role of Endothelial Autocrine NRG1/ERBB4 Signaling in Cardiac Remodeling

(Submitter supplied) Neuregulin-1 (NRG1) is a paracrine growth factor, secreted by cardiac endothelial cells (Ecs) in conditions of cardiac overload/injury. The current concept is that the cardiac effects of NRG1 are mediated by activation of ERBB4/ERBB2 receptors on cardiomyocytes. However, recent studies have shown that paracrine effects of NRG1 on fibroblasts and macrophages are equally important. Here, we hypothesize that NRG1 autocrine signaling plays a role in cardiac remodeling. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
24 Samples
Download data: TSV
Series
Accession:
GSE150619
ID:
200150619
11.

Transcriptome Analysis of Zfpm1 Function in Early Zebrafish Embryogenesis and Postembryonic Heart Development

(Submitter supplied) Through analyzing RNA-seq datasets in zfpm1 mutant embryo (36hpf) and maturing heart (21 dpf), we characterized the effects of loss of zfpm1 on the transcriptomic landscape.
Organism:
Danio rerio
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23085
8 Samples
Download data: TXT
Series
Accession:
GSE95118
ID:
200095118
12.

Single-cell analysis uncovers that metabolic reprogramming is essential for cardiomyocyte proliferation in the regenerating heart.

(Submitter supplied) While the heart regenerates poorly in mammals, efficient heart regeneration occurs in certain amphibian and fish species. Zebrafish has been used extensively to study heart regeneration, resulting in a model in which preexisting cardiomyocytes dedifferentiate and reinitiate proliferation to replace the lost myocardium. However, there is limited knowledge about the cellular processes that occur in this rare population of proliferating cardiomyocytes during heart regeneration. more...
Organism:
Danio rerio
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20828
4 Samples
Download data: CSV, TSV
Series
Accession:
GSE139218
ID:
200139218
13.

Myocardial Bmp2 overexpression leads to ectopic cardiac EMT and promotes chamber cardiomyocyte proliferation and immaturity

(Submitter supplied) Defective valve and septa formation constitute a substantial part of congenital heart defects affecting the neonate or the adult. During cardiac development, restricted myocardial Bmp2 expression is a key signal for the specification and patterning of the valve-forming field in the atrio-ventricular canal (AVC) region and the initiation of the epithelial-mesenchyme transition (EMT) that gives rise to the valve primordia. more...
Organism:
Mus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23658
5 Samples
Download data: TXT
Series
Accession:
GSE100810
ID:
200100810
14.

Prerequisite endocardial-mesenchymal transition for cardiac trabecular angiogenesis

(Submitter supplied) We used single cell RNA sequencing (scRNAseq) to show that ventricular endocardial cells generate trabecular vessels through an angioEMT mechanism.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
7 Samples
Download data: MTX, TSV
Series
Accession:
GSE205394
ID:
200205394
15.

Activated YAP1 stimulates cardiomyocyte proliferation

(Submitter supplied) Postnatal day 4 neonatal rat cardiomyocytes transduced with LacZ or flag-tagged, activated YAP1 (S127A) expressing adenovirus After transduction, cells were cultured in serum free media and collected 48 hours later.
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platform:
GPL6247
8 Samples
Download data: CEL
Series
Accession:
GSE33019
ID:
200033019
16.

ERBB2 drives YAP activation and EMT-like processes during cardiac regeneration

(Submitter supplied) RNA-seq comparing WT and caERBB2 over expresising hearts with/out injury
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
16 Samples
Download data: XLSX
Series
Accession:
GSE144391
ID:
200144391
17.

Endocardial/endothelial angiocrines regulate cardiomyocyte development and maturation and induce features of ventricular non-compaction

(Submitter supplied) Non-compaction cardiomyopathy is a devastating genetic disease caused by insufficient consolidation of ventricular wall muscle that can result in inadequate cardiac performance. Despite being the third most common cardiomyopathy, the mechanisms underlying the disease, including the cell types involved, are poorly understood. We have previously shown that endothelial cell-specific deletion of the chromatin remodeller gene Ino80 results in defective coronary vessel development that leads to ventricular non-compaction in embryonic mouse hearts. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
2 Samples
Download data: H5
Series
Accession:
GSE175589
ID:
200175589
18.

Profiling of INO80-regulated transcription

(Submitter supplied) We performed RNA-seq of primary human umbilical vein cells (HUVEC) before and after knockdown of Ino80 with siRNA
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: CSV, XLSX
19.

Endocardial HDAC3 is required for myocardial trabeculation [bulk RNA-seq]

(Submitter supplied) To investigate the growth factors regulated in the endocardial cells, we performed gene expression profiling analysis using RNA-Seq data obtained from Hdac3 CRISPR knockout mouse cardiac endothelail cells
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
8 Samples
Download data: TXT
Series
Accession:
GSE229677
ID:
200229677
20.

Endocardial HDAC3 is required for myocardial trabeculation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
Platforms:
GPL21103 GPL19057
22 Samples
Download data: TAR
Series
Accession:
GSE229661
ID:
200229661
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