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Links from GEO DataSets

Items: 10

1.

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
2.

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drug and agonist of the peroxisome proliferator-activated receptor gamma (Pparg), rosiglitazone, was recently withdrawn in many countries because the drug use was associated with an increased risk of heart failure.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
3.

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
4.

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
5.

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
6.
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
7.

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
8.

Expression data from adult (9 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates

(Submitter supplied) G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE41706
ID:
200041706
9.

Cardiomyocyte HIPK2 Maintains Basal Cardiac Function via ERK Signaling

(Submitter supplied) Background: Cardiac kinases play a critical role in the development of heart failure, and represent potential tractable therapeutic targets. However, only a very small fraction of the cardiac kinome has been investigated. To identify novel cardiac kinases involved in heart failure, we employed an integrated transcriptomics and bioinformatics analysis and identified Homeodomain-Interacting Protein Kinase 2 (HIPK2) as a novel candidate kinase. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
9 Samples
Download data: CEL
Series
Accession:
GSE136308
ID:
200136308
10.

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
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