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. 2017 Nov 29;7:291. doi: 10.3389/fonc.2017.00291

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Copyright © 2017 Dahl and Aird.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Ataxia-telangiectasia mutated (ATM) modulates cellular metabolism. DNA damage activates ATM to phosphorylate multiple downstream proteins regulate cell cycle arrest, DNA repair, and apoptosis pathways. A non-canonical function of ATM is the regulation of cellular metabolism. Mitochondrial ATM acts to regulate mitochondrial homeostasis by repairing mitochondrial genome defects. ATM activates the tumor suppressor p53, which inhibits GLUT recruitment, glycolysis, and dNTP production. Consistently, p53 targets the oncogene c-myc, inhibiting the TCA cycle and increasing the Warburg effect. In addition, ATM activates AKT to increase GLUT recruitment to the membrane.