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. 2018 Jun 22;8:9511. doi: 10.1038/s41598-018-27864-6

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© The Author(s) 2018

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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GRAMD1B inhibition increases Akt signaling. (a) Inhibitory effects of GRAMD1B on PI3K/Akt signaling. Gramd1b knockdown results in a dramatic increase in p-Akt levels but fails to alter p-PI3K levels, suggesting that GRAMD1B acts downstream to PI3K but upstream/parallel to Akt. Full-length blots are included in Supplementary Fig. S9. (b) The morphology changes of Gramd1b knockdown cells are negated in the presence of the pan-Akt inhibitor MK-2206. (Scale bar = 20 μm). (c-c’) MK-2206 treatment suppresses the GRAMD1B inhibition-enhanced cell migration. (Scale bar = 100 μm). Data is represented as mean ± SEM of n = 3. (d) Treatment of cells with MK-2206 significantly inhibits the expression of Rac1 and Cdc42 induced by Gramd1b knockdown. Data is represented as mean ± SEM of n = 3. *P < 0.05; ***P < 0.001.