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. 2018 Feb 20;8:5. doi: 10.1186/s13395-018-0150-5

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 8 — Model of Nilotinib effects on myoblasts and skeletal myogenesis. Nilotinib binds to and inhibits p38 MAPK. Consequently, Nilotinib activates the MEK/ERK proliferation signaling inhibiting myoblast differentiation. Simultaneously, Nilotinib stimulates the AKT survival pathway. In addition, ERK1/2 and AKT stimulation is required for Nilotinib-induced myoblast proliferation. The stimulation of proliferation and the anti-myogenic effects of Nilotinib through the perturbation of p38, ERK, and AKT signaling pathways are illustrated