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. 2014 Jul 31;5(7):e1358. doi: 10.1038/cddis.2014.316

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Copyright © 2014 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/

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Elevation of Bid in response to ALDH1L1 is associated with JNK-dependent protection from degradation. (a) Levels of Bid mRNA are not changed in response to ALDH1L1. (b) Bid is not degraded upon etoposide treatment in ALDH1L1-expressing PC-3 cells. siRNA silencing of JNK1/2 (c), but not the canonical JNK1/2 downstream target c-Jun (d), prevents Bid accumulation in response to ALDH1L1 (in this experiment, samples generated in the previous study²⁵ were reanalyzed; the efficiency of c-Jun silencing is shown in that publication). (e and f) JNK1/2 silencing by siRNA inhibits ALDH1L1-induced apoptosis and protects PC-3 cells from the ALDH1L1 cytotoxic effect. Average of two independent experiments is shown for apoptotic cells; MTT assays were performed with six replicates. Difference between numbers of live cells at 72 h is highly statistically significant (P<0.0001, indicated by *)