Figure 1.

Schematic illustration of autophagy regulation. Autophagy is an intracellular mechanism by self-digestion and recycling damaged components in response to various stresses, including nutrient deprivation. Under stress conditions, mTOR is suppressed, and autophagy-related proteins are activated for the formation, growth, and closure of the isolation membrane, in which ATG5 is essential. The ATG5 is required for the lipidation of LC3 from LC3-I to LC3-II. The LC3-II is the only protein that exists on the completed double-membraned isolation membrane, autophagosome. Then, matured autophagosomes that incorporate their own surplus protein and waste products are degraded by the fusion with the lysosome, leading to the production and reuse of amino acids. The p62/SQSTM1 serves as a link with LC3, and its labeled proteins are selectively degraded in this process. Monitoring this dynamic process, autophagic flux, is essential for understanding autophagy regulation. In this study, autophagy was inhibited at the early stage by RNAi using ATG5 siRNA or at the late stage by lysosomotropic chloroquine supplementation.