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. 2019 Jan 28;5:60. doi: 10.1038/s41420-019-0139-9

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© The Author(s) 2019

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. 7 — At low concentrations (≤0.2 µM) in aRMS and eRMS cells AJ-5 induces DSBs leading to increased levels of γH2AX and activation of both the canonical DSB pathway (ATM/Chk2) and the p38/MAPK stress signalling pathway. This results in a p21-induced G₁ cell cycle arrest followed by the activation of the extrinsic and intrinsic apoptotic pathways and a reduction in autophagic flux