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. 2022 Oct 27;5:1141. doi: 10.1038/s42003-022-04097-y

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — Major signaling networks involved in PKB/Akt-mTORC1-mediated muscle proteostasis in control mice (wild type, upper left), with sustained mTORC1 activity (TSCmKO, upper right), sustained mTORC1 activity and Nrf1-kd-mediated proteasome depletion (lower left) and sustained mTORC1 activity with constitutive PKB/Akt activation (lower right). Impairing ubiquitin-proteasome-mediated protein breakdown under conditions with high mTORC1 activity disrupts proteostasis and leads to unhealthy muscles, independent of muscle growth status. Figure created with BioRender.com.