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. 2020 Jun 18;11:243. doi: 10.1186/s13287-020-01766-9

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 5 — The expressions of p-Erk1/2 and p-Smad2 in the human ES cells treated with M6 without/with small molecular inhibitors. a The expression of total/phosphorylation Erk1/2 and total/phosphorylation Smad2 when treated with P13 and its mutant M6 without any inhibitor. b The expressions of the TGFβ signaling pathways after being treated with TGFβ receptor inhibitors (LDN-193189, SB431542, and A8301); the concentration of SB431542 was 1.0 and 10 μmol, and the concentration of A8301/LDN-193189 was 0.2 and 1.0 μmol. c The expression of the FGFR pathways after being treated with FGFR receptor inhibitors (AZD4547 and PD173074); the concentration of AZD4547 was 0.2 μmol, and the concentration of PD173074 was 1.0 μmol. d The expressions of the FGF and TGFβ signaling pathways after being treated with the FGFR and TGFβ receptor dual inhibitors (0.2 μmol AZD4547 and 1.0 μmol A8301)