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. 2018 Nov 12;25:80. doi: 10.1186/s12929-018-0465-x

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 5 — Graphical abstract. Our results revealed a novel mechanism whereby Axl binds and phosphorylates TNS2 at Y483, releasing TNS2 from interacting with IRS-1, resulting in increased stability of IRS-1. Higher levels of IRS-1 may enhance cellular glucose uptake through up-regulation of Glut 4 and cell growth and survival. The two key enzymes of aerobic glycolysis, PDK1 was found to be up-regulated by the Axl/TNS2/IRS-1 cross-talk. The details of this regulatory cross-talk remain to be elucidated