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. 2017 Mar 16;8(3):e2668. doi: 10.1038/cddis.2017.37

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Copyright © 2017 The Author(s)

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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PrP^C is involved in RhoA inactivation in the brains of three different types of mice. (a) Detection of RhoA-GTP levels in the brains of C57BL/6J (BL6, WT), Tga20 (Tga, PrP overexpression) and Zürich I (Zu, PrP-deficient) mice (n=3 per each group). (b) Phosphorylation of RhoA, LIMK, and cofilin was assessed in the whole-brain lysates of C57BL/6J, Tga20, and Zürich I mice. The data are expressed as the mean±S.E. of three independent experiments (*P<0.05, **P<0.01, ***P<0.001, n=3)