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. 2015 Dec 21;1:15063. doi: 10.1038/cddiscovery.2015.63

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Copyright © 2015 Cell Death Differentiation Association

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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Schematic representation of the mechanism of AMPK-mediated cell survival. AMPK is activated under glucose-limiting conditions as well as by AICAR. AMPK, by increasing p-p38 and by inhibiting mTOR, regulates expression of PGC-1α which controls mitochondrial biogenesis in cancer cells and allows oxidative metabolism of non-glucose carbon sources (glutamine, lactate and fatty acids) to generate ATP. To restore ATP pool, AMPK enhances metabolic rate by activating PFK2.