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. 2017 Aug 3;8(8):e2965. doi: 10.1038/cddis.2017.353

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Copyright © 2017 The Author(s)

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Schematic of the AcSDKP/FGFR1/MAP4K4 pathway suppression of TGFβ/smad signaling and EndMT. In endothelial cells, the close proximity between AcSDKP and FGFR1 increased FGFR1 and induced its phosphorylation levels. Interacting with co-factor FRS2, FGFR1 recruited MAP4K4 and induced its phosphorylation. Subsequently, p-MAP4K4 suppressed integrinβ1 (integrinβ1 should be localized on the cell surface interacted with some of α integrins). Integrinβ1 was a potent activator of TGF-β signaling and also EndMT. Therefore, AcSDKP could inhibit EndMT through FGFR1-MAP4K4-dependent manner