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. 2022 Jan 10;13:114. doi: 10.1038/s41467-021-27684-9

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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. 9 — Acp5 is upregulated by TGF-β1 in a TGFβR1/Smad3 depend manner, and then Acp5 specially binds to p-β-catenin and dephosphorylate the sites of Ser33 and Thr41, by which it resists the degradation of β-catenin and enhanced β-catenin signaling in the nuclear to promote the differentiation, proliferation and migration of fibroblasts.