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Literature summary for 1.8.4.11 extracted from

  • Moskovitz, J.; Du, F.; Bowman, C.F.; Yan, S.S.
    Methionine sulfoxide reductase A affects beta-amyloid solubility and mitochondrial function in a mouse model of Alzheimer's disease (2016), Am. J. Physiol. Endocrinol. Metab., 310, E388-E393 .
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine mouse model of Alzheimer's disease, a mouse that overexpresses amyloid precursor protein and Abeta in neurons. Lack of MsrA fosters the formation of methionine sulfoxide in proteins. MsrA-deficient mice expressing amyloid precursor protein exhibit higher levels of soluble Abeta in brain. Mitochondrial respiration and the activity of cytochrome c oxidase are compromised in the MsrA-deficient mice expressing amyloid precursor protein compared with control mice Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining

Organism

Organism UniProt Comment Textmining
Mus musculus
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General Information

General Information Comment Organism
physiological function mouse model of Alzheimer's disease, a mouse that overexpresses amyloid precursor protein and Abeta in neurons. Lack of MsrA fosters the formation of methionine sulfoxide in proteins. MsrA-deficient mice expressing amyloid precursor protein exhibit higher levels of soluble Abeta in brain. Mitochondrial respiration and the activity of cytochrome c oxidase are compromised in the MsrA-deficient mice expressing amyloid precursor protein compared with control mice Mus musculus