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. 2018 Nov 21;26(9):1582–1599. doi: 10.1038/s41418-018-0226-0

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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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Fig. 8 — Vps26a-mediated neurogenesis depends on cooperation between Nox, ROS, and the ERK1/2 cascade. a, b The effects of oxidant treatment on modulation of pERK1/2, pp38 MAPK, pJNK, and pAKT levels were determined by western blot analysis using WT (+/+) and Vps26a^-/- (-/-) ESCs or shCTL (shC)- and shVps26a (shV)-ECCs (b) treated with increasing concentrations of hydrogen peroxide (50 and 100 μM), respectively, for 10 min at the end of neural differentiation (6 days). a–i, b–i Immunoblotting quantification of (a) and (b). Western blot signals were quantified and the intensity of phosphorylated protein and the total protein normalized to the loading control GAPDH are presented (n = 3 for each group). Error bars are ± SD. ^**P < 0.01; ^***P < 0.001 vs. +/+ ND 6 (a–i) and shCTL ND 6 (b–i). c, d The effects of antioxidant- and Nox inhibitor treatments on modulation of pERK1/2, pp38 MAPK, pJNK, and pAKT levels were determined by western blot analysis using WT and Vps26a^-/- ESCs (c) or shCTL- and shVps26a-ECCs (d) cultured in the presence or absence of 20 mM NAC or 2.5 μM DPI for 6 h at the end of neural differentiation (6 days and 144 h, respectively). c–i, d–i Immunoblotting quantification of (c) and (d). Western blot signals were quantified and the intensity of phosphorylated protein and the total protein normalized to the loading control GAPDH are presented (n = 3 for each group). Error bars are ± SD. ^***P < 0.001 vs. +/+ ND 6 (c–i) and shCTL ND 6 (d–i). e Immunocytochemical analysis of pERK1/2 using WT and Vps26a^-/- ESCs differentiated in the presence or absence of 20 mM NAC or 2.5 μM DPI for 6 days. Scale bar, 50 μm. f, g The effect of ERK1/2 inhibitor treatment on ROS generation examined by fluorescence microscopy (f) or flow cytometry (g) using +/+ and -/- ESCs differentiated in the presence or absence of PD98059 for 3 days. Error bars indicate the means ± SD (n = 3). ^***P < 0.001. h The effect of ERK inhibitor treatment on the expression of Nox4 determined by semi-qPCR analysis using +/+ and -/- ESCs differentiated in the presence or absence of PD98059 for 6 days