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. 2016 Oct 31;2:16076. doi: 10.1038/cddiscovery.2016.76

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Copyright © 2016 The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International 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/4.0/

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Role of caspase-2 in apoptosis induced by etoposide or gemcitabine. Mouse cells expressing E1A 12S (a) or human cells expressing genomic E1A (b) were treated with etoposide or gemcitabine in the absence (black bars) or presence (gray bars) of the caspase-2-specific inhibitor, zVDVAD (200 μM) for 18 h, and specific Cr⁵¹ release was determined (mean±S.E.M.; n=3, ***P<0.001). (c) E1A 12S-positive mouse cells (E1A) or caspase-2 siRNA-expressing E1A 12S-positive mouse cells (E1AiC2) were treated with the chemical NO generator, DETANoNoate (NO) (250 μM), TNFα (20 ng/ml), etoposide (400 μM) or gemcitabine (50 μM) for 18 h, and specific Cr⁵¹ release was determined (mean±S.E.M.; n=3, ***P<0.001).