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Journal Article

A guide to the regulation of selective autophagy receptors


Đikić,  Ivan       
Institute of Biochemistry II, Faculty of Medicine, Goethe University Frankfurt, Frankfurt, Germany;
Max Planck Fellow Group ER remodelling Group, Prof. Ivan Đikić, Max Planck Institute of Biophysics, Max Planck Society;
Buchmann Institute for Molecular Life Sciences, Goethe University Frankfurt, Frankfurt, Germany;

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Gubas, A., & Đikić, I. (2022). A guide to the regulation of selective autophagy receptors. The FEBS Journal, 289(1), 75-89. doi:10.1111/febs.15824.

Cite as: https://hdl.handle.net/21.11116/0000-0008-4C58-1
Autophagy is a highly conserved catabolic process cells use to maintain their homeostasis by degrading misfolded, damaged and excessive proteins, nonfunctional organelles, foreign pathogens and other cellular components. Hence, autophagy can be nonselective, where bulky portions of the cytoplasm are degraded upon stress, or a highly selective process, where preselected cellular components are degraded. To distinguish between different cellular components, autophagy employs selective autophagy receptors, which will link the cargo to the autophagy machinery, thereby sequestering it in the autophagosome for its subsequent degradation in the lysosome. Autophagy receptors undergo post-translational and structural modifications to fulfil their role in autophagy, or upon executing their role, for their own degradation. We highlight the four most prominent protein modifications - phosphorylation, ubiquitination, acetylation and oligomerisation - that are essential for autophagy receptor recruitment, function and turnover. Understanding the regulation of selective autophagy receptors will provide deeper insights into the pathway and open up potential therapeutic avenues.