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. 2021 Oct 27;10(10):72. doi: 10.1038/s41389-021-00361-8

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© The Author(s) 2021, corrected publication 2021

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. 6 — IDH1 mutation suppressed the TGF-β signaling pathway and E2F4 interacted with Smad3 to inhibit expression of mesenchymal markers in the proneural subtype of GBM. However, palmitoylation of Smad3 mediated by palmitoyltransferase ZDHCH19 promoted activation of the TGF-β signaling pathway and its interaction with EP300 to promote expression of mesenchymal markers in the mesenchymal subtype of GBM. GBM glioblastoma, IDH1 isocitrate dehydrogenase 1.