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. 2015 Jun 4;6(6):e1779. doi: 10.1038/cddis.2015.151

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Copyright © 2015 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 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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IL-1β activates p53 through an oxidative stress-dependent mechanism. (a) NPCs were cultured in unconditioned stem cell media (Ctrl) or LPS/γIFN-aMCM in the presence or absence of N-acetylcysteine (5 mM). Protein was extracted at 48 h and p53, Puma, p21 and actin expression was assayed by western blot. Representative immunoblots and densitometric analysis from three independent experiments is shown (n=3; *P<0.05). (b) NPCs were treated with rIL-1β (50 ng/ml) or left untreated (Ctrl) and protein was extracted after 48 h and assayed for p53, p21 and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) expression by western blot. Representative immunoblots and densitometric analysis from three independent experiments is shown (n=3, *P<0.05)