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. 2017 Dec 14;23(46):8109–8119. doi: 10.3748/wjg.v23.i46.8109

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©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

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Proposed model for the bi-directional IGF1R signaling-dependent modulation of the autophagic pathway. IGF1R targeting via suppression of the "canonical" PI3K/Akt/mTORC1 pathway stimulates the autophagy process. However, it can also result in a reduced formation of autophagosomal precursors at the plasma membrane. IGF1R depletion inhibits mTORC2, which reduces the activity of protein kinase C alpha and beta. This finally negatively impacts autophagosome precursor formation. IGF1R: Insulin-like growth factor receptor 1; PI3K: Phosphatidylinositol-3-kinase; AKT: Serine/threonine kinase, named protein kinase B (PKB); mTORC1/2: Mammalian target of rapamycin complex 1/2; PKC: Protein kinase C; ATG16L1: Autophagy-related protein 16-1.