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. 2017 Oct 16;7:13201. doi: 10.1038/s41598-017-13501-1

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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The biological function of csMVP is mediated through the control of mTOR, FAK, ERK and Akt signaling. (a) Western blot analysis of MVP, Akt1/2/3 and ERK1/2 in Huh7 cells treated with rIgG or α-MVP. The phosphorylation of Akt1/2/3 and ERK1/2 was also examined in Huh7 cells treated with rIgG or α-MVP. The signal intensities of Western blots were measured quantitatively using the Image J software, and GAPDH was used as a loading control. (b) Western blot analysis of MVP, S6, FAK in Huh7 cells treated with rIgG or α-MVP. The phosphorylation of S6 and FAK was also examined in Huh7 cells treated with rIgG or α-MVP. β-actin was used as a loading control.