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. 2020 Apr 15;30(9):779–793. doi: 10.1038/s41422-020-0309-6

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© Center for Excellence in Molecular Cell Science, CAS 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 — Vascular endothelial cells release s-HBEGF upon sorafenib stimulation. s-HBEGF binds to EGFR and leads to JNK2 phosphorylation in keratinocytes. The activated JNK2 subsequently stabilizes SIRT1, which eventually results in keratinization. The classic SIRT1 inhibitor nicotinamide could effectively reverse sorafenib-induced HFSR.