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The non-enzymatic mitochondrial protein hyperacetylation induced by the increased availability of mitochondrial acetyl-CoA avoids the risk associated with mitochondria overfeeding, restraining the activity of the respiratory complex I and modulating CACT activity

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For comparison, we treated cells with tunicamycin (TUN, a widely-used ER stress inducer) which did not alter phospho-GCN2 (T899), but reduced the mobility of PERK, indicative of its increased phosphorylation (Fig