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. 2015 Jun 18;6(6):e1790. doi: 10.1038/cddis.2015.154

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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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AMPK activation is required for IL-1β-induced loss of SERCA2 protein expression. INS-1 cells (a and b), isolated rat islets (c) or non-diabetic cadaveric human islets (d) were transduced with an HA-tagged AMPK-DN or DN or control adenovirus (Luci or Lu) before 24- h treatment with or without 5 ng/ml IL-1β (for INS-1 cells and rat islets) or a combination of 5 ng/ml IL-1β, 1 ng/ml TNFα and 100 ng/ml IFN-γ in human islets. Total protein was isolated, and immunoblot was performed using antibodies against SERCA2, pAMPKα, total AMPKα, phosphorylated ACC (pACC), total ACC, HA and actin. (b) Quantitative protein levels of SERCA2 in INS-1 cells are shown graphically. Indicated comparisons are significantly different (**P<0.01)