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• W2001388306 abstract "We set out to determine whether cellular hypoxia, via mitochondrial reactive oxygen species, promotes Na,K-ATPase degradation via the ubiquitin-conjugating system. Cells exposed to 1.5% O 2 had a decrease in Na,K-ATPase activity and oxygen consumption. The total cell pool of α1 Na,K-ATPase protein decreased on exposure to 1.5% O 2 for 30 hours, whereas the plasma membrane Na,K-ATPase was 50% degraded after 2 hours of hypoxia, which was prevented by lysosome and proteasome inhibitors. When Chinese hamster ovary cells that exhibit a temperature-sensitive defect in E1 ubiquitin conjugation enzyme were incubated at 40°C and 1.5% O 2 , the degradation of the α1 Na,K-ATPase was prevented. Exogenous reactive oxygen species increased the plasma membrane Na,K-ATPase degradation, whereas, in mitochondrial DNA deficient ρ 0 cells and in cells transfected with small interfering RNA against Rieske iron sulfur protein, the hypoxia-mediated Na,K-ATPase degradation was prevented. The catalase/superoxide dismutase (SOD) mimetic (EUK-134) and glutathione peroxidase overexpression prevented the hypoxia-mediated Na,K-ATPase degradation and overexpression of SOD1, but not SOD2, partially inhibited the Na + pump degradation. Accordingly, we provide evidence that during hypoxia, mitochondrial reactive oxygen species are necessary to degrade the plasma membrane Na,K-ATPase via the ubiquitin-conjugating system." @default.
• W2001388306 created "2016-06-24" @default.
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• W2001388306 date "2006-05-26" @default.
• W2001388306 modified "2023-10-12" @default.
• W2001388306 title "Hypoxia-Mediated Degradation of Na,K-ATPase via Mitochondrial Reactive Oxygen Species and the Ubiquitin-Conjugating System" @default.
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• W2001388306 doi "https://doi.org/10.1161/01.res.0000222418.99976.1d" @default.
• W2001388306 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16614303" @default.
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