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. 2016 Apr 30;16:35. doi: 10.1186/s12935-016-0310-9

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© Hayashi et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 4 — YS110 augments phosphorylation of p38MAPK and ERK1/2. a Activating phosohorylation of p38 (Thr180/Tyr182) and ERK1/2 (Thr202/Tyr204) were elevated by 24 h after treatment with YS110 while no substantial changes of whole p38 and ERK1/2 protein were observed. β-actin was used as an internal control. b G2/M arrest caused by YS110 treatment was reversed by ERK1/2 activation inhibitor U0126 (10 μM). A proportion (43.15 %) of G2/M was elevated in cells with YS110 treatment compared with in cells without YS110 (control, 37.05 %) and the proportion of G2/M decreased in cells with both YS110 and U0126 treatment (35.06 %). All experiments were performed in triplicate and a representative experiment is shown