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Links from GEO DataSets

Items: 14

1.

CHF1/Hey2 Promotes Physiological Hypertrophy in response to Pressure Overload

(Submitter supplied) We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
8 Samples
Download data: CEL
Series
Accession:
GSE13031
ID:
200013031
2.

Transcription Factor CHF1/Hey2 Regulates Specific Gene Sets in Serum Stimulated Primary Cardiac Myocytes

(Submitter supplied) Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
25 Samples
Download data: CEL
Series
Accession:
GSE14288
ID:
200014288
3.

Expression time course data HEY2 KO and WT MASMC treated with PDGF

(Submitter supplied) The cardiovascular restricted transcription factor CHF1/Hey2 has been previously shown to regulate the smooth muscle response to growth factors. To determine how CHF1/Hey2 affects the smooth muscle response to growth factors, we performed a genomic screen for transcripts that are differentially expressed in wild type and knockout smooth muscle cells after stimulation with platelet derived growth factor. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS2704
Platform:
GPL1261
16 Samples
Download data: CEL
Series
Accession:
GSE6526
ID:
200006526
4.
Full record GDS2704

Transcription factor CHF1/Hey2 null smooth muscle cell response to platelet-derived growth factor: time course

Analysis of CHF1/Hey2 null aortic smooth muscle cells treated for up to 480 minutes with platelet-derived growth factor (PDGF). CHF1/Hey2 is a cardiovascular transcription factor. Results provide insight into the mechanisms regulated by CHF1/Hey2 in the response of smooth muscles to growth factors.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 agent, 2 genotype/variation, 8 time sets
Platform:
GPL1261
Series:
GSE6526
16 Samples
Download data: CEL
DataSet
Accession:
GDS2704
ID:
2704
5.

Loss of heat shock protein HSPA4 aggravates pressure overload-induced myocardial damage

(Submitter supplied) Failure of molecular chaperones to direct the correct folding of newly synthesized proteins leads to the accumulation of misfolded proteins in cells. HSPA4 is a member of the heat shock protein 110 family (HSP110) that acts as a nucleotide exchange factor of HSP70 chaperones. We found that the expression of HSPA4 is upregulated in murine hearts subjected to pressure overload and in failing human hearts. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL13730
6 Samples
Download data: CEL
Series
Accession:
GSE32885
ID:
200032885
6.

Elevated Myocardial Na+/H+ Exchanger Elicits the Expression of Genes that Lead to Cardiac Hypertrophy

(Submitter supplied) In myocardial disease, elevated expression and activity of Na+/H+ exchanger isoform 1 (NHE1) is detrimental. To better understand the involvement of NHE1, transgenic mice with elevated heart-specific NHE1 expression were studied. N-line mice expressed wild-type NHE1 and K-line mice expressed activated NHE1. Cardiac morphology, interstitial fibrosis and cardiac function were examined by histological staining and echocardiography. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6481
9 Samples
Download data: TXT
Series
Accession:
GSE19819
ID:
200019819
7.

Analysis of Akt1 activation in transgenic mouse hearts show expression profiles associated with hypertrophy and failure

(Submitter supplied) To investigate molecular mechanisms involved in the development of cardiac hypertrophy and heart failure, a tetracycline-regulated transgenic system to conditionally switch a constitutively-active form of the Akt1 protein kinase on or off in the adult heart was developed. Short-term activation (2 weeks) of Akt1 resulted in completely reversible hypertrophy with maintained contractility. In contrast, chronic Akt1 activation (6 weeks) induced extensive cardiac hypertrophy, severe contractile dysfunction, and massive interstitial fibrosis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Datasets:
GDS2304 GDS2308
Platforms:
GPL340 GPL339
36 Samples
Download data
Series
Accession:
GSE3383
ID:
200003383
8.
Full record GDS2308

Akt1 serine-threonine protein kinase activation effect on the heart (MG-430B)

Analysis of hearts after acute or chronic induction of a transgenic Akt1 kinase. Acute activation results in reversible hypertrophy, while chronic activation induces transition to failure. Results provide insight into the mechanisms involved in the development of cardiac hypertrophy and failure.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 5 protocol sets
Platform:
GPL340
Series:
GSE3383
18 Samples
Download data
DataSet
Accession:
GDS2308
ID:
2308
9.
Full record GDS2304

Akt1 serine-threonine protein kinase activation effect on the heart (MG-430A)

Analysis of hearts after acute or chronic induction of a transgenic Akt1 kinase. Acute activation results in reversible hypertrophy, while chronic activation induces transition to failure. Results provide insight into the mechanisms involved in the development of cardiac hypertrophy and failure.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 5 protocol sets
Platform:
GPL339
Series:
GSE3383
18 Samples
Download data
DataSet
Accession:
GDS2304
ID:
2304
10.

Gene expression profile of cells from Hey2 enhancer-LacZ transgenic (Tg) mouse embryos at embryonic day (E) 7.5.

(Submitter supplied) We used single cell RNA sequencing (scRNA-seq) to analyze cells that activate the Hey2 enhancer in mouse embryos at E7.5.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL28457
1 Sample
Download data: MTX, TSV, TXT
Series
Accession:
GSE227506
ID:
200227506
11.

Kdm3a in mouse promotes pressure overload induced cardiac hypertrophy

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
12 Samples
Download data
Series
Accession:
GSE120740
ID:
200120740
12.

Kdm3a in mouse promotes pressure overload induced cardiac hypertrophy [WT vs. KO]

(Submitter supplied) Heart disease and failure is a leading cause of mortality worldwide. Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular morbidity and mortality and the development of heart failure. Pathological LVH induced by sustained pressure-overload engages transcriptional programs including reactivation of canonical fetal genes and those inducing fibrosis. Histone lysine demethylases (KDMs) are emerging potent regulators of transcriptional reprogramming in cancer, though their potential role in abnormal growth and fibrosis in heart disease remains little understood. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
6 Samples
Download data: TXT
Series
Accession:
GSE120739
ID:
200120739
13.

Kdm3a in mouse promotes pressure overload induced cardiac hypertrophy [WT vs. Tg]

(Submitter supplied) Heart disease and failure is a leading cause of mortality worldwide. Left ventricular hypertrophy (LVH) and myocardial fibrosis are the major risk factor for cardiovascular morbidity and mortality and the development of heart failure. Pathological LVH induced by sustained pressure-overload engages transcriptional programs including reactivation of canonical fetal genes and those inducing fibrosis. Histone lysine demethylases (KDMs) are emerging potent regulators of transcriptional reprogramming in cancer, though their potential role in abnormal growth and fibrosis in heart disease remains little understood. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
6 Samples
Download data: TXT
Series
Accession:
GSE120737
ID:
200120737
14.

Kdm3a in mouse promotes pressure overload induced cardiac hypertrophy [RNA-seq]

(Submitter supplied) Heart disease and failure is a leading cause of mortality worldwide. Left ventricular hypertrophy (LVH) and myocardial fibrosis are major risk factors for cardiovascular morbidity and mortality and the development of heart failure. Pathological LVH induced by sustained pressure-overload engages transcriptional programs including reactivation of canonical fetal genes and those inducing fibrosis. Histone lysine demethylases (KDMs) are emerging potent regulators of transcriptional reprogramming in cancer, though their potential role in abnormal growth and fibrosis in heart disease remains little understood. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
4 Samples
Download data: XLSX
Series
Accession:
GSE120598
ID:
200120598
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