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. 2018 Dec 17;9:5343. doi: 10.1038/s41467-018-07741-6

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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. 9 — Chronic or acute inhibition of cysteine or aspartyl cathepsins lead to a similar response. a Levels of P-STAT3 and CtsD in WT MEFs treated or not with 10 μM E64 or 5 μM Pepstatin A for 72 h. Data are the average ± SD of n = 4 biologically independent samples for P-STAT3 and n = 3 biologically independent samples for CtsD. Statistical significance was calculated using a two-sided unpaired t-test. b Levels of P-STAT3, STAT3, CtsD and SOD1 in CtsB^−/− heart or CtsL^−/− heart compared to WT heart. Data are the average ± SD of n = 3 biologically independent samples. Statistical significance was calculated using a two-sided unpaired t-test