Cells are constantly challenged by endogenous and exogenous stress sources. To cope with them, organisms have developed a series of defensive mechanisms to prevent and intercept the threats and to repair the generated damage. Autophagy, once defined as a waste-disposal or non-specific degradative pathway, has arisen as a new organizer of the different physiological stress responses. In the present review, we will discuss how autophagy is capable of orchestrate these pathways by the specific degradation of individual autophagosomal LC3/GABARAP-binding proteins, rather than the bulk degradation of harmful products or organelles.
Keywords: CRY1; NCoR1; TRIM5; autophagy; p62/SQSTM1.
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