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. 2021 Jul 8;12:678974. doi: 10.3389/fphys.2021.678974

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Copyright © 2021 Rossi, Falzarano, Osman, Armaroli, Scotton, Mantuano, Boccanegra, Cappellari, Schwartz, Yuryev, Mercuri, Bertini, D’Amico, Mora, Johansson, Al-Khalili Szigyarto, De Luca and Ferlini.

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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Pathway for circadian rhythm regulation in skeletal muscles and its effect on muscle differentiation and atrophy. Genes that are downregulated in mdx mice more than 2-fold are shown in blue, genes upregulated more than 2-fold are shown in red. Pathway Studio analysis shows that downregulation of the ARNTL1 gene leads to upregulation of MYOG, which is known to be involved in muscle atrophy due to increased expression of ubiquitin ligases TRIM63 and FBXO32, rather than being a clear marker of ongoing regeneration. The ARNTL1-CLOCK1 complex is also repressed by upregulation of the Timeless protein that directly binds and represses CLOCK1, and by downregulation of CSNK1E that activates ARNTL1 directly by phosphorylation and through destabilization of PER1/2 proteins.