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Literature summary for 2.3.1.61 extracted from

  • Dumont, M.; Ho, D.J.; Calingasan, N.Y.; Xu, H.; Gibson, G.; Beal, M.F.
    Mitochondrial dihydrolipoyl succinyltransferase deficiency accelerates amyloid pathology and memory deficit in a transgenic mouse model of amyloid deposition (2009), Free Radic. Biol. Med., 47, 1019-1027.
    View publication on PubMedView publication on EuropePMC

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrion
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Homo sapiens 5739
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Organism

Organism UniProt Comment Textmining
Homo sapiens
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male transgenic Tg19959 mice (model of amyloid deposition, 2 mutations in the human amyloid precursor protein) are crossed with dihydrolipoyl succinyltransferase deficient female mice (DLST+/-)
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Synonyms

Synonyms Comment Organism
dihydrolipoyl succinyltransferase
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Homo sapiens
DLST
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Homo sapiens

General Information

General Information Comment Organism
malfunction reduced enzyme activity increases H2O2-induced reactive oxygen species production and cell death, in human Alzheimer disease brains the activity of the alpha-ketoglutarate dehydrogenase enzyme complex is reduced, enzyme deficient mice show increased plaque burden, Abeta oligomers, and nitrotyrosine levels, the occurrence of spatial learning and memory deficits in female Tg19959 mice is accelerated Homo sapiens
physiological function key subunit of the alpha-ketoglutarate dehydrogenase enzyme complex, involved in NADH production, participation in oxidative stress and reactive oxygen species (ROS) production Homo sapiens