Ontology highlight
ABSTRACT:
PROVIDER: PRJNA733914 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description: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. The pathological changes in our model were compatible with human cardiac aging. To investigate the transcriptional alterations in the mutant heart, we carried out an Affymetrix microarray analysis for comparison between the mutant and normal heart at 16 weeks of age. Keywords = Mn-SOD Keywords = manganese superoxide dismutase Keywords = knockout Keywords = heart failure Keywords = heart Keywords = muscle Keywords: parallel sample
2005-02-05 | GSE2236 | GEO
Project description:The accumulation of α-synuclein (ASyn) has been observed in several lysosomal storage diseases (LSD), but it remains unclear if the accumulation of ASyn contributes to the pathology. The mitochondria degeneration, reduced expression of manganese superoxide dismutase 2, and reactive oxygen species-mediated oxidative damage were observed in the neurons of Hexb-/- mice.
2015-05-12 | GSE68748 | GEO
Project description:The accumulation of α-synuclein (ASyn) has been observed in several lysosomal storage diseases (LSD), but it remains unclear if the accumulation of ASyn contributes to the pathology. The mitochondria degeneration, reduced expression of manganese superoxide dismutase 2, and reactive oxygen species-mediated oxidative damage were observed in the neurons of Hexb-/- mice. Gene expression in the brain of 14-week-old Hexb-/- ASyn+/+, Hexb-/- Asyn-Tg, and Hexb-/- ASyn-/- mice were analyzed.
2015-05-12 | E-GEOD-68748 | biostudies-arrayexpress
Project description: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. We show that SOD2, which normally binds manganese, can incorporate iron and generate an alternative isoform with peroxidase activity. The switch from manganese to iron allows FeSOD2 to utilize H2O2 to promote oxidative stress. We found that FeSOD2 is formed in cultured cells. FeSOD2 causes mitochondrial dysfunction and higher levels of oxidative stress in cultured cells. We show that formation of FeSOD2 converts an antioxidant defense into a prooxidant peroxidase that leads to cellular changes seen in multiple human diseases.
2017-12-05 | GSE106206 | GEO
Project description:Switch of mitochondrial superoxide dismutase into a prooxidant peroxidase in manganese-deficient cells
| PRJNA415919 | ENA
Project description:Grad-seq in Enterococcus faecalis V583 and Enterococcus faecium AUS004.
2022-11-28 | PXD031577 | Pride
Project description:Manganese is considered essential for animal growth. Manganese ions serve as cofactors to three mitochondrial enzymes: superoxide dismutase (Sod2), arginase and glutamine synthase. In Drosophila melanogaster, manganese has also been implicated in the formation of ceramide phosphoethanolamine, the insect’s sphingomyelin analogue, a structural component of membranes. Manganese overload leads to neurodegeneration and toxicity in both humans and Drosophila. Here, we describe a Drosophila model of manganese deficiency. Due to the lack of manganese-specific chelators, we used chemically defined media to grow the flies and deplete them of the metal. Dietary manganese depletion reduces Sod2 activity. We then examined gene and protein expression changes in the intestines of manganese depleted flies. We found adaptive responses to the lack of the known manganese-dependent enzymatic activities and alterations in genes/enzymes of carbohydrate metabolism and glycosylations, similar to earlier reports of manganese deficiency in vertebrate animals.
2020-02-24 | PXD015543 | Pride
Project description:Young adult N2 Caenorhabditis elegans were infected with Enterococcus faecalis or Enterococcus faecium for 8 h to determine the transcriptional host response to each enterococcal species. Analysis of differential gene expression in C. elegans young adults exposed to four different bacteria: heat-killed Escherichia coli strain OP50 (control), wild-type E. faecalis MMH594, wild-type E. faecium E007, or Bacillus subtilis PY79 (sigF::kan). Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Brain-heart infusion agar plates (10 ug/ml kanamycin) were used.
2018-02-14 | GSE95636 | GEO
Project description:Effect of 20 ug/ml ampicillin on gene expression of Enterococcus faecium E1162 during mid-exponential growth phase
2012-03-01 | E-MEXP-3564 | biostudies-arrayexpress
Project description:Proteomic Characterization of Bacteriocin-Producing Enterococcus faecium Strains from foodstuffs
2023-03-11 | PXD037241 | Pride