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. 2018 Jul 24;8:43. doi: 10.1186/s13578-018-0242-2

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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. 2 — Roles of MCM phosphorylation mediated by p56Lyn, Akt and ILK in cancer development. Phosphorylation of MCM7 mediated by EGFR-p56^Lyn and RACK1-Akt promotes MCM complex assembly and chromatin loading, therefore enhancing DNA synthesis and cancer cell proliferation. In contrast, MCM7 phosphorylation mediated by ITGA7-ILK axis reduces MCM7 chromatin association, inhibiting cell growth