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. 2018 May 22;9(6):596. doi: 10.1038/s41419-018-0624-8

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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 — a Speed profiles of H_CT carriers in wild-type motor neurons treated with DMSO (black squares), SOD1^G93A motor neurons treated with DMSO (red diamonds) and SOD1^G93A motor neurons treated with 2 μM SB-203580 (blue triangles). Comparison of the curves reveals SOD1^G93A motor neurons treated with 2 μM SB-203580 have a similar speed distribution to wild-type cultures (wild type: 134 carriers, 16 axons; SOD1^G93A: 112 carriers, 12 axons; SOD1^G93A + 2 μM SB-203580: 75 carriers, 10 axons; 3 independent experiments). b Speed distribution profiles of H_CT carriers in wild-type motor neurons treated with DMSO (black squares), SOD1^G93A motor neurons treated with DMSO (red diamonds) and SOD1^G93A motor neurons treated with 2 μM SB-239063, a p38 MAPKα and β specific inhibitor (blue triangles). Comparison of the speed profiles reveals SOD1^G93A motor neurons treated with 2 μM SB-239063 have a similar speed distribution curve to wild-type cultures (wild type: 134 carriers, 16 axons; SOD1^G93A: 112 carriers, 12 axons; SOD1^G93A + 2 μM SB-239063: 85 carriers, 9 axons; 3 independent experiments). c–f The rescue of deficits in the axonal transport of signal endosomes by SB-239063 is independent of JNK inhibition. Wild type (WT) and SOD1^G93A motor neuron lysates were blotted and stained for active phosphorylated JNK (p-JNK) and for total JNK (c). The ratio of these signals shown in (e) is not significantly affected by treatment with 2 μM SB-239063. These samples were stained for phosphorylated p38 MAPK (p-p38 MAPK), total p38 MAPKα and GAPDH as loading control (d). The ratio of p-p38 MAPK / total p38 MAPKα signals shown in (f) reveals a significant inhibition of p38 MAPK upon SB-239063 treatment even in conditions maximising p38 MAPK activation (0.5 μ./ml anisomycin for 60 min; see Fig. 3). n = 3 independent experiments; data shown as mean ± SEM. *, p < 0.05 (two-way ANOVA)