Autophagy involves the lysosomal degradation of cytoplasmic contents for regeneration of
anabolic substrates during nutritional or inflammatory stress. Its initiation occurs rapidly after
inactivation of the protein kinase mammalian target of rapamycin (mTOR)(or mechanistic
target of rapamycin), leading to dephosphorylation of Unc-51-like kinase 1 (ULK1) and
autophagosome formation. Recent studies indicate that mTOR can, in parallel, regulate the
activity of stress transcription factors, including signal transducer and activator of …