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. 2020 Nov 23;11:5938. doi: 10.1038/s41467-020-19721-w

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© The Author(s) 2020

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 — Left panel: wild-type ETNK1 actively phosphorylates Et leading to the accumulation of P-Et, which in turn negatively modulates mitochondrial activity and ROS production through inhibition of SDH. Middle panel: in the presence of mutated ETNK1 the production of P-Et is impaired, which causes abnormal mitochondrial activation, increased ROS production and DNA damage. Right panel: treatment of ETNK1-mutated cells with exogenous P-Et leads to restoration of normal mitochondrial activity through suppression of SDH, normalization of ROS production and protection of DNA from ROS-mediated damage. Elements of the image were obtained from https://smart.servier.com/ under a Creative Commons Attribution 3.0 License.