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These findings suggest that YAP1 might not be a direct substrate of CDK4/6 and that an unidentified intermediary factor may mediate the regulation of YAP1 by CDK4/6

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More specifically, in mammalian cells, cyclin D3-Cdk6 kinase complexes phosphorylate and inactivate the key glycolytic enzymes PFKP and PKM2 to shunt glycolytic intermediates toward NADPH and GSH production, which mitigates ROS accumulation to promote cell survival (Wang et al., 2017)

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