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Links from GEO DataSets

Items: 20

1.

Whole genome cardiac gene expression profiling of transgenic mice with myocardium-specific expression of RKIP (PEBP1), kinase-inactive GRK2-K220R (ADRBK1-K220R), SCD1, and UCP1

(Submitter supplied) The raf kinase inhibitor protein, RKIP, is up-regulated on cadiac biopsy specimens of heart failure patients. To investigate the in vivo role of an increased cardiac content of RKIP, we generated transgenic mice with myocardium-specific expression of RKIP (PEBP1; phosphatidylethanolamine binding protein 1) under control of the alpha-MHC promoter in B6 (C57BL/6J) background. Because RKIP is a dual-specific GRK2 and Raf kinase inhibitor, RKIP-transgenic mice were compared to transgenic mice with myocardium-specific expression of the GRK2 inhibitor, GRK2-K220R, which is a kinase-inactive GRK2 (ADRBK1) mutant with dominant-negative function. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
10 Samples
Download data: CEL, CHP
Series
Accession:
GSE120020
ID:
200120020
2.

Model of heart failure induced by mild thiol-blocking with cystamine

(Submitter supplied) Depletion of cardiac ATP content is a characteristic feature of heart failure in patients and experimental animal models. To analyze the impact of insufficient ATP supply on heart function we inhibited cellular respiration by disulfide poisoning with the mild thiol-blocking agent, cystamine. We chose 4 month-old apolipoprotein E (apoE)-deficient mice, which are highly vulnerable to increased oxygen and ATP demands. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE25768
ID:
200025768
3.

Cardiac gene expression profiling of apoE-deficient mice receiving heart failure treatment with the anti-ischemic drug ranolazine

(Submitter supplied) Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We used 18 month-old apolipoprotein E (apoE)- deficient mice as a model of atherosclerosis-induced heart failure to analyze whether the anti-ischemic drug ranolazine could retard the progression of heart failure. The study showed that 2 months of ranolazine treatment improved cardiac function of 18 month-old apoE-deficient mice with symptoms of heart failure as assessed by echocardiography. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE25767
ID:
200025767
4.

Cardiac gene expression profiling of heart failure treatment with the anti-ischemic drug ranolazine

(Submitter supplied) Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We analyzed whether the anti-ischemic drug ranolazine could retard the progression of heart failure in an experimental model of heart failure induced by 6 months of chronic pressure overload. The study showed that 2 months of ranolazine treatment improved cardiac function of aortic constricted C57BL/6J (B6) mice with symptoms of heart failure as assessed by echocardiography. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE25766
ID:
200025766
5.

Microarray gene expression profiling of cardiac genes at the onset of heart failure

(Submitter supplied) Atherosclerosis and pressure overload are major risk factors for the development of heart failure in patients. Cardiac hypertrophy often precedes the development of heart failure. However, underlying mechanisms are incompletely understood. To investigate pathomechanisms underlying the transition from cardiac hypertrophy to heart failure we used experimental models of atherosclerosis- and pressure overload-induced cardiac hypertrophy and failure, i.e. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
18 Samples
Download data: CEL, CHP
Series
Accession:
GSE25765
ID:
200025765
6.

Whole genome microarray gene expression profiling of peripheral blood mononuclear cells (PBMC) isolated from old and middle-aged, voluntary human research participants

(Submitter supplied) With increasing age of the global population, age-associated diseases such as cardiovascular diseases, cancer or diabetes are on the rise in many countries. To identify cellular processes and markers of aging in humans, this study performed comparative whole genome microarray gene expression profiling of peripheral blood mononuclear cells (PBMC) isolated from two age groups, i.e., an old age group (age: 75-89 years) and a younger, middle-aged group (age: 35-50 years). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
9 Samples
Download data: CEL, CHP
Series
Accession:
GSE237029
ID:
200237029
7.

Cardiac transcriptome analysis of RKIP-transgenic and GRK2-transgenic mice by NGS

(Submitter supplied) The RAF kinase inhibitor protein, RKIP, is a dual inhibitor of the RAF1 kinase and the G-protein-coupled receptor kinase 2 (GRK2). By inhibition of the proto-oncogenic and pro-survival RAF1-MAPK pathway, the RAF kinase inhibitor protein, RKIP, acts as a tumor suppressor, which enhances cardiomyocyte death and promotes the development of symptoms of heart failure. To elucidate pathomechanisms of heart failure induced by RKIP, the study determined the cardiac transcriptomes of eight-month-old, male, transgenic mice with cardiac-specific expression of RKIP (PEBP1) under control of the myocardium-specific, alpha-MHC promoter. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
9 Samples
Download data: TXT
Series
Accession:
GSE191316
ID:
200191316
8.

Microarray gene expression profiling of kinase-dependent and kinase-independent effects of GRK2

(Submitter supplied) The ubiquitously expressed G-protein-coupled receptor kinase 2 (GRK2, ADRBK1) is an indispensable kinase involved in growth, differentiation and development. Exaggerated GRK2 activity plays a major pathophysiological role in the development of cardiovascular diseases such as heart failure and hypertension. GRK2 exerts its functions by kinase-dependent and kinase-independent effects. To assess the differential impact of GRK2 on cellular signalling we established HEK cell clones with over-expression of comparable protein levels of GRK2 or the kinase-deficient GRK2-K220R mutant, respectively. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4544
Platform:
GPL570
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE42771
ID:
200042771
9.

Microarray gene expression profiling of transgenic mice with myocardium-specific expression of RKIP or a GRK-specific peptide inhibitor

(Submitter supplied) The Raf kinase inhibitor protein (RKIP) is a dual inhibitor of the Raf kinase and the G-protein-coupled receptor kinase 2 (GRK2). GRK2 is an indispensable kinase, which exerts a major role in the pathogenesis of heart failure, and inhibition of GRK2 is cardioprotective in experimental models of heart failure. To investigate the cardiac function of RKIP as GRK2 inhibitor, we generated transgenic mice with myocardium-specific expression of RKIP under control of the alpha-MHC promoter. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE42753
ID:
200042753
10.
Full record GDS4544

G-protein-coupled receptor kinase 2 inhibition effect on HEK cells in vitro and in vivo

Analysis of HEK cells expressing dominant-negative GRK2-K220R. HEK cells were cultured, or expanded in NOD.Scid mice, or re-cultured after NOD.Scid expansion. GRK2-K220R enhances growth of NOD.Scid HEK cells but not cultured HEK cells. Results provide insight into basis of growth control by GRK2.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 genotype/variation, 3 protocol sets
Platform:
GPL570
Series:
GSE42771
12 Samples
Download data: CEL, CHP
11.

Microarray gene expression profiling of transgenic mice with myocardium-specific over-expression of fatty acid synthase (FASN)

(Submitter supplied) The fatty acid synthase (FASN) is the major fat synthesizing enzyme. FASN is an indispensable enzyme because mice with genetic deletion of Fasn are not viable. Apart from its physiological function, previous studies indicated that FASN could also exert a pathophysiological role, in the heart, because patients with heart failure showed up-reguation of FASN. To investigate the in vivo function of FASN up-regulation in the heart, we generated mice with myocardium-specific expression of FASN under control of the alpha-MHC promoter. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE49351
ID:
200049351
12.

Microarray gene expression profiling of heart failure induced in apolipoprotein E-deficient mice by treatment with rosiglitazone

(Submitter supplied) The anti-diabetic drug and agonist of the peroxisome proliferator-activated receptor gamma (Pparg), rosiglitazone, was recently withdrawn in many countries because the drug use was associated with an increased risk of heart failure. To investigate underlying pathomechanisms, we chose 6-month-old apolipoprotein E (apoE)-deficient mice, which are prone to atherosclerosis and insulin resistance, and thereby mimic the risk profile of patients with cardiovascular disease. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE28031
ID:
200028031
13.

Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure

(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
Platforms:
GPL13112 GPL21103
17 Samples
Download data: GTF, HIC, NARROWPEAK
Series
Accession:
GSE96693
ID:
200096693
14.

Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [HiC-seq]

(Submitter supplied) Understanding the principles of endogenous chromatin structure has key implications for epigenetic therapy. To determine the mechanisms of genome structure-function in post-mitotic cells, genome-wide chromatin conformation capture was performed in cardiac myocytes, a non-dividing, differentiated cell responsible for cardiac contraction. Cardiac-specific CTCF knockout mice demonstrated that loss of CTCF had minimal effect on topologically associating domains; however, it selectively altered boundary strength and A/B compartmentalization, with gene expression changes mimicking those in heart failure. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL21103
3 Samples
Download data: HIC
Series
Accession:
GSE96692
ID:
200096692
15.

Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [ChIP-seq]

(Submitter supplied) Understanding the principles of endogenous chromatin structure has key implications for epigenetic therapy. To determine the mechanisms of genome structure-function in post-mitotic cells, genome-wide chromatin conformation capture was performed in cardiac myocytes, a non-dividing, differentiated cell responsible for cardiac contraction. Cardiac-specific CTCF knockout mice demonstrated that loss of CTCF had minimal effect on topologically associating domains; however, it selectively altered boundary strength and A/B compartmentalization, with gene expression changes mimicking those in heart failure. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: NARROWPEAK
Series
Accession:
GSE96691
ID:
200096691
16.

Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [RNA-seq]

(Submitter supplied) Understanding the principles of endogenous chromatin structure has key implications for epigenetic therapy. To determine the mechanisms of genome structure-function in post-mitotic cells, genome-wide chromatin conformation capture was performed in cardiac myocytes, a non-dividing, differentiated cell responsible for cardiac contraction. Cardiac-specific CTCF knockout mice demonstrated that loss of CTCF had minimal effect on topologically associating domains; however, it selectively altered boundary strength and A/B compartmentalization, with gene expression changes mimicking those in heart failure. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
10 Samples
Download data: GTF
Series
Accession:
GSE96690
ID:
200096690
17.

Gene expression profiles in Sirt1/PPARalpha bigenic mice

(Submitter supplied) Cardiac-specific PPARalpha transgenic (Tg-PPARalpha) mice show mild cardiac hypertrophy and systolic dysfunction. The failing heart phenotypes observed in Tg-PPARalpha are exacerbated by crossing with cardiac-specific Sirt1 transgenic (Tg-Sirt1) mice, whereas Tg-Sirt1 mice themselves do not show any cardiac hypertrophy or systolic dysfunction. To investigate the mechanism leading to the failing heart phenotypes in TgPPARalpha/Tg-Sirt1 bigenic mice, microarray analyses were performed. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
8 Samples
Download data: CEL
Series
Accession:
GSE33101
ID:
200033101
18.

RNA-seq on parental and acquired resistant cells (AqR)

(Submitter supplied) Parental and AqR cells were obtained at diferent time-points (Day1 and Day 18). Total RNA was extracted and submitted for RNA-seq. Differential expression was observed between parental and AqR cells. AqR cells were derived from parental cells by adding inhibitor (CAY10566) every 3 days until cells became resistant (at about 3 weeks).
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: XLSX
19.

ATAC-seq on parental and acquired resistant cells (AqR)

(Submitter supplied) Parental and AqR cells were obtained. DNA was purified and submited for sequencing. Differential chromatin accessiblity was observed. AqR cells were derived from parental cells by adding inhibitor (CAY10566) every 3 days until cells became resistant (at about 3 weeks).
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
2 Samples
Download data: BED
Series
Accession:
GSE130638
ID:
200130638
20.

Transcriptome analysis of valosin-containing protein effect on cardiac hypertrophy and dysfunction

(Submitter supplied) This sstudy was designed to investigate the gene netweork regulated by valosin-containing protein (VCP), an ATPase-associated protein, whic acts as a novel regulator against the cardiac stress of pressure overload. We performed transcriptome analyses to compare cardiac-specific VCP overexpression transgenic (TG) mice and wild-type (WT) mice in a series of pathological models. The left ventricular (LV) tissues were collected from both WT and VCP TG mice at 2w post TAC and at 2w post sham operations. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
22 Samples
Download data: CSV
Series
Accession:
GSE134085
ID:
200134085
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