GEO DataSets

Analysis of hearts from C57BL/6 mutants lacking manganese superoxide dismutase (MnSOD). MnSOD deficiency confined to heart and muscle. Mutants developed progressive congestive heart failure with dilated cardiomyopathy. Results provide insight into the effect of excess oxidative stress on the heart.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE2236

4 Samples

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(Submitter supplied) To investigate the pathological significance of excess oxidative stress in the heart, we generated heart/muscle-specific manganese superoxide dismutase (MnSOD) -deficient mice on a C57BL/6 background using the Cre-loxP system uder the control of the muscle reatin kinase (MCK) promoter. The mutant mice developed progressive congestive heart failure with dilated cardiomyopathy and physical disability and died with a median survival rate of 15.4 ± 4.0 weeks. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS1080

Platform:

GPL1261

4 Samples

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(Submitter supplied) Transcriptional microarray analysis was conducted on gastrocnemius muscle of control and PGC-1β(i)skm-/- mice one week after the last tamoxifen administration using the Affymetrix Mouse Gene 1.0 ST.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

2 Samples

Download data: CEL, CHP

(Submitter supplied) Superoxide radical anion and other Reactive Oxygen Species are constantly produced during respiration. In mitochondria, the dismutation of the superoxide radical anion is accelerated by the mitochondrial superoxide dismutase 2 (SOD2), an enzyme that has been traditionally associated with antioxidant protection. However, increases in SOD2 expression promote oxidative stress, indicating that there may be a prooxidant role for SOD2. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

12 Samples

Download data: TXT

(Submitter supplied) Myocardial deletion of klf4 sensitizes mouse to pressure overload. In order to gain a better understanding of molecular mechanisms of such alterations, we profiled gene expression before and after 3-day of pressure overload (induced by transverse aortic constriction -TAC) in the hearts from MHC-cre (Cre) control and MHC-cre-klf4-deficient (KO) mice.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL7202

15 Samples

Download data: TXT