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. 2015 Aug 27;6(8):e1865. doi: 10.1038/cddis.2015.239

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Copyright © 2015 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 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/4.0/

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MiR-26a-GSK3β regulate axon regeneration by controlling Smad1 expression. (a) Representative western blot images of Smad1 in cultured adult mouse sensory neurons 3 days after inhibition of miR-26a. (b) Quantification of Smad1 level (normalized to actin, n=3). (c) Representative western blot images of Smad1 in cultured adult mouse sensory neurons 3 days after inhibition of miR-26a with or without the treatment the GSK3 inhibitor BIO. (d) Quantification of Smad1 level (normalized to actin, n=3). (e) Representative images of cultured adult mouse sensory neurons expressing EGFP, EGFP+miR-26a inhibitor (anti-26a), Smad1 and Smad1+anti-26a. Scale bar=100 μm. (f) Quantification of the average length of the longest axons (normalized to the average length of the control axons, n=3). Bar graphs are shown as means±S.E.M. **P<0.005