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The knockout and inhibition of c-MYC reduces the expression of SIRT1 through binding to two potential c-MYCbinding sites (E-boxes E1 and E2) of the SIRT1 promoter
Impeding mitochondrial function is also prospective
doi: 10.1038/nchembio807
MOTS-cs demonstrated ability to enhance both glucose utilization and fatty acid oxidation positions it as a potential modulator of this flexibility
It is plausible that the majority, or even all, of these CGIs function as sites for transcription initiation
