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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. 5 — Vps26a involves Nox expression during neurogenesis. a, b The effect of Vps26a deficiency and knockdown on the expression of the Nox family was determined by semi-qPCR (a) and qPCR (b) analyses using shCTL (shC)- and shVps26a (shV)-ECCs, differentiated for the indicated time periods. Error bars indicate the means ± SD (n = 3). ^**P < 0.01; ^***P < 0.001 compared with shCTL-ECCs each day. c Overview of Vps26a and Nox4 immunostaining of a sagittal section of WT and Vps26a^-/- mouse embryos (E10.5) counterstained lightly with hematoxylin. Scale bar , 200 µm. d Double-label immunocytochemical analysis of Oct3/4 and Nox4 using WT and Vps26a^-/- ESCs differentiated for 6 days. DAPI staining data are shown as insets to the merged images. Scale bar, 50 μm. e Expression of Nox4, Oct3/4, and Nox4 in WT and Vps26a^-/- teratomas. Scale bar, 100 μm