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. 2018 Oct 8;28(11):1090–1102. doi: 10.1038/s41422-018-0086-7

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — PKM2 is over-expressed in cancer where it unites cancer glycolytic metabolism with DNA repair to drive treatment resistance. PKM2 is frequently overexpressed in cancer cells where cytosolic PKM2 reprograms glucose metabolism (Warburg effect), while nuclear PKM2 has additional oncogenic function as a transcriptional coactivator (black arrows). Our data uncovered a novel nuclear function of PKM2 through which it directly regulates DNA DSB repair and resistance to genotoxic damage (red arrows). ATM, activated by DNA DSBs, phosphorylates nuclear PKM2 at T328, resulting in nuclear retention and accumulation of PKM2. pT328-PKM2 interacts with CtIP and phosphorylates CtIP on T126 to increase its function in HR repair, resulting in increased DSB repair efficiency and resistance to genotoxic treatments