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Consistent with the specific ATF4 target genes induced by mTORC1 signaling, including those involved in amino acid acquisition and tRNA charging, we found that ATF4 activation contributes to both canonical (e.g., protein synthesis) and new (e.g., glutathione synthesis) functions of mTORC1

neurofeedback based on improving self-control over brain activity patterns (real-time electroencephalogram (EEG) data monitoring of, for example, theta (vigilance) and beta (concentration and neuronal excitability waves) [26,27,28]

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