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. 2017 Aug 25;7:9438. doi: 10.1038/s41598-017-09633-z

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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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HGF-promoted Akt phosphorylation and cell proliferation are impaired in Pip5K1a ^−/− hepatocytes. Primary hepatocytes prepared from adult Pip5k1a ^+/+ (control) and Pip5k1a ^−/− mice were stimulated with 10 ng/mL of HGF for the indicated time, and Akt phosphorylation (a) and cell proliferation (b) were assessed as in Fig. 1e and d, respectively. Phosphorylation of c-Met and Erk (a) were also assessed as in Fig. 1g. Quantitative results represent means ± SEM from at least three independent experiments. Scale bar, 50 μm. Statistical analyses: two-way ANOVA with post hoc Bonferroni’s test. ***p < 0.001. Blots shown in (a) are cropped images. The full-length blots are presented in Supplementary Figure.