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. 2020 Aug 25;10:14151. doi: 10.1038/s41598-020-70822-4

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© The Author(s) 2020

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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TRPV4 regulates Cdc42/N-wasp axis in glioblastoma cells. (A–B) Pull-down and western blot assays showing Cdc42/N-wasp axis activation in U87 cells treated with antagonist (50 nM or 100 nM) or agonist (5 nM or 10 nM). (C) Western blot assays show the knockdown effect of two sequences of sh-Cdc42 in U87 cells. (D) The activation of N-wasp was detected by western blot after knockdown Cdc42 or combined with GSK2 and GSK1. (E) Western blot analysis of the activation of the Cdc42/N-wasp axis after ML141 (Cdc42 inhibitor, 500 nM) treatment or combined with TRPV4 agonist. (F) The activation of N-wasp was detected by western blot assay after treatment with wiskostatin (N-wasp inhibitor, 5 µM) without or with TRPV4 agonist. *p < 0.05, **p < 0.01.