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. 2021 Mar 11;9:656201. doi: 10.3389/fcell.2021.656201

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Copyright © 2021 Zimmermann, Madreiter-Sokolowski, Stryeck and Abdellatif.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Autophagy core machinery. Upstream nutrient/growth factor signaling and cellular energy status regulate mTORC1 and AMPK kinases, respectively, which in turn inhibit or activate ULK1 through different phosphorylation sites. ULK1 phosphorylates components of the phagophore formation machinery, consisting of a class III PI3K complex, ATG12-ATG5-ATG16 complex, ATG9, and LC3-II. LC3-II can interact with cargo (e.g., protein aggregates) through cargo receptors such as SQSTM1/p62 or organelles like mitochondria through mitochondrial surface markers. ATG3 and ATG7 mediate ATG12-ATG5 and LC3-PE conjugation. SIRT1 deacetylates and activates several ATG proteins. See text for details. Abbreviations: LC3-II, microtubule-associated protein light chain 3 (lipidated form); PE, phosphatidylethanolamine; PI3K, phosphatidylinositol 3 kinase; ULK1, Unc-51-like kinase 1.