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. 2018 May 29;8:8234. doi: 10.1038/s41598-018-26481-7

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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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Effect of MG132 treatment on wild-type and CHM3 iPSC-derived RPE. (A) Western blot analysis of REP1 expression following treatment of wild-type iPSC-derived RPE with increasing concentrations of MG132. β-actin serves as a loading control. Bands were cropped from the same gel with different exposure times for REP1 and β-actin. (B) Quantification of REP1 expression in panel A shows an increase at all concentrations used with the highest levels observed at 2 µM (~5-fold higher than non-treated (NT) cells). Western blot analysis of REP1 expression in non-treated (NT), DMSO-treated or PTC124-treated CHM3 iPSC-derived RPE in the absence (C) or presence (D) of MG132. β-actin serves as a loading control. No expression could be seen in CHM3 iPSC-derived RPE as compared to wild-type (WT) RPE regardless of the treatment used. In panels C and D, bands were cropped from the same gel with different exposure times for REP1 and β-actin.