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Molecular remedy of complex I defects: rotenone-insensitive internal NADH-quinone oxidoreductase of Saccharomyces cerevisiae mitochondria restores the NADH oxidase activity of complex I-deficient mammalian cells
Moreover, most of the glutathionylated proteins studied are cytosolic and not much is known about what happens in other cellular compartments
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Our strategy involved rigorous bioinformatic analysis of transcriptional changes within this time frame to make inferences about the signals and transcription factors known to regulate the affected biological processes
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