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. 2021 Jul 19;9:127. doi: 10.1186/s40478-021-01228-0

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — VPS4, but not CHMP4B nor CHMP2B, is increased in C9orf72 and sALS postmortem motor cortex neuronal nuclei. a, b Maximum intensity projections from SIM imaging of CHMP4B, CHMP2B, and VPS4 in nuclei isolated from postmortem control, C9orf72, and sALS motor (a) and occipital (b) cortex tissue. Genotype as indicated on left, brain region and antibody as indicated on top. c–e Quantification of CHMP4B (c), CHMP2B (d), and VPS4 (e) spots. n = 6 control, 6 C9orf72, and 9 sALS cases, 50 NeuN + nuclei per line/brain region. One-way ANOVA with Tukey’s multiple comparison test was used to calculate statistical significance. ****p < 0.0001. Scale bar = 5 μm