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. 2020 Sep 17;11(9):773. doi: 10.1038/s41419-020-02986-w

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© The Author(s) 2020

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. 3 — a Left, representative scheme of the AKT/mTORC1 pathway. Right, western blot of the components of the pathway in LA1-5s and SK-N-BE(2) cell lines treated with the indicated ABTL0812 concentrations for 24 h. b Western blot quantification. Graph represents the mean of two out of three independent experiments. Band intensity was normalised to GAPDH and vehicle-treated cells. *p ≤ 0.05, compared to vehicle. c Left, representative scheme of the UPR PERK pathway. Right, western blot of the components of the pathway in LA1-5s and SK-N-BE(2) cell lines treated with the indicated ABTL0812 concentrations for 0, 3, 6 and 8 h. d Graph represents the mean quantification of two out of three independent experiments. Band intensity was normalised to GAPDH and time 0 h. *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001 compared to time = 0.