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. 2017 May 8;7:1564. doi: 10.1038/s41598-017-01696-2

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© The Author(s) 2017

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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ER stress leads to a disruption in the lysosomal membrane. MIA PaCa-2 cells analyzed for lysosome membrane permeabilization. (A) Cells treated with 1 μM tunicamycin and analyzed for cytosolic cathepsin B activity. (B) Cells treated with 1 μM tunicamycin, and stained with cathepsin B and lysotracker. Images taken at 60x magnification. (C) Cells treated with 100 nM mithramycin and analyzed for cytosolic cathepsin B activity. (D) Cells treated with 100 nM mithramycin, and stained with cathepsin B and lysotracker. Images taken at 60x magnification. (E) Viability determined for cells treated with 100 nM mithramycin or 1 μM tunicamycin, with and without a cathepsin B inhibitor, Ca074me. (F) Cells treated with 1 μM tunicamycin, with and without Ca074me detected by immunofluorescence. Images taken at 40x and 60x magnification.