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. 2019 Oct 29;9:15557. doi: 10.1038/s41598-019-51914-2

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© The Author(s) 2019

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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Aβ-induced RhoA hyperactivation and the accumulation of F-actin are dependent on SHIP2 activity. (a,b) Representative images (a) and the averaged values (b) of the FRET/CFP emission ratio images of RhoA biosensor in the HT22 cells stimulated with 1 μM of Aβ in the absence or presence of 10 μM AS09 for 24 hr (means ± SEM; t-test; *p < 0.05; n = 40~42 cells per group). (c) Active RhoA was quantified using ELISA-based RhoA activation assay (means ± SEM; t-test; *p < 0.05; n = 4). (d,e) Representative images (d) and the quantified intensity (e) of lifeact-mCardinal in HT22 cells treated with 1 μM Aβ in the absence or presence of 10 μM AS09 for 24 hr (means ± SEM; t-test; *p < 0.05; n = 80~88 cells per group). (f,g) Representative images (f) and the quantification analysis (g) of phalloidin after the stimulation with 1 μM of Aβ for 24 hr in HT22 cells overexpressing ARAP3 or R982A mutant (means ± SEM; t-test; *p < 0.05; n = 32~40 cells per group).