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. 2016 Jun 29;7:274. doi: 10.3389/fphys.2016.00274

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Copyright © 2016 Zhong, Li, Li, Sun, Cao, Li, Zhao, Song, Jin, Song, Yuan, Wu, Li, Xu, Kan, Cao, Ling and Li.

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) or licensor 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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Activity of signaling pathways in the mouse heart following hindlimb unloading and recovery. (A,F) Representative western blots of HDAC4 and its phosphorylation at Ser246, AMPKα and its phosphorylation at Thr172, ERK1/2, and its phosphorylation at Thr202/Tyr204, and LC3 of the left ventricle (LV) and right ventricle (RV). Gapdh levels served as a loading control. Quantification of phosphorylation levels normalized to total protein (LC3-II levels normalized to LC3-I levels) of the LV (B–E) and RV (G–J). (K) Summary of changed signaling molecules. HDAC4, Histone Deacetylase 4; ERK, Extracellular Regulated Protein Kinases; AMPK, AMP-activated Protein Kinase; LC3, Microtubule-associated Protein Light Chain 3. Gapdh, Glyceraldehyde phosphate dehydrogenase. Values are means ± SEM (n = 4). ^*P < 0.05, ^**P < 0.01, ^***P < 0.001.