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doi: 10.1146/annurev-nutr-071816-064732 51 RomanoKAVivasEIAmador-NoguezDReyFE
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232 The deletion of S6K1 in mouse embryonic fibroblasts enhances mitochondrial fission by increasing both total DRP1 and its S616-phosphorylated form (not a target of S6K1 but a substrate of PINK1, CDK1 and other kinases), which in turn stimulates glycolysis
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