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. 2016 Jun 17;23(10):1658–1669. doi: 10.1038/cdd.2016.56

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Copyright © 2016 Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

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E2F1 increases the transcription of miR-17-92 in myoblasts. (a–c) E2F1 protein expression during C2C12 myoblast myogenesis (a), mouse muscle regeneration (b) and postnatal growth (c). Beta-actin and beta-tubulin served as the loading controls. (d) Overexpression of miR-17, -20a or -92a reduces E2F1 protein expression in C2C12 myoblasts transfected with the miR-17, -20a or -92a mimics. The data are presented as the means of the samples from three different cell samples. M1, mouse 1; M2, mouse 2. Beta-actin served as the loading control