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mTORC1, which is well known for its function at the center of cancer metabolic reprogramming, promotes mitochondrial glutaminolysis via the migration of SIRT4-mediated inhibition of GLUD1 189

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Such binding may displace other regulatory proteins, making DNA more accessible for transcriptional machinery, potentially inducing neuronal cell differentiation in retinal and periodontal ligament stem cells (hPDLSCs)

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Furthermore, studies have confirmed eye-related symptoms