This context dependence also suggests that, when applying BCAA-related targets for disease intervention, it is necessary to distinguish between two different levels of regulatory modes: the mTOR-driven pro-inflammatory effects caused by enhanced BCAA uptake/transport, and the support provided by changes in BCAA catabolic flux to mitochondrial metabolism and reparative programs, so as to avoid conflating results obtained from different experimental systems
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The EGCG could have also exerted cell cycle arrest by causing a significant decrease in the expression of CDK4 and PCNA (Zhang et al., 2010a
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