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Dexamethasone (Dex)-mediated cell death is associated with repression of survival factors (AP-1, c-myc, NF-kappaB). Dex suppressed the activity of genes encoding antioxidant enzymes leading to impaired viability and apoptotic cell death. These findings suggest that reactive oxygen species inhibit protein synthesis and amplify m-calpain-dependent proteolysis. The events that led to death of L6 muscle cells were most likely triggered by Dex-mediated repression of antioxidative defenses on the genomic level.
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Orzechowski et al. (2003) studied this question.
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