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. 2022 Sep 21;54(9):1549–1562. doi: 10.1038/s12276-022-00849-2

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© The Author(s) 2022

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. 5 — a Immunohistochemical staining of ALK5 in LF tissues from the two groups (n = 6). The scale bar indicates 100 μm. b Quantitative analysis of the positive cell ratio for ALK5. Data are shown as the mean ± S.D. **P < 0.01. c, d Reciprocal immunoprecipitation showing the interaction between ALK5 and CLU. LF cells were treated with 5 ng/ml TGF-β1 for 24 h before performing Co-IP analysis. e Representative images from the immunofluorescence assay showing the colocalization of ALK5 and CLU after treatment with 5 ng/ml TGF-β1 using specific antibodies. ALK5 (green), CLU (red) and DAPI (blue). The scale bar indicates 50 μm. f Western blot analysis showed the effects of ALK5 overexpression on the SMAD3 signaling pathway protein levels upon treatment with TGF-β1 and CLU or not. g Effects of siALK5 on the protein levels of the SMAD3 signaling pathway upon treatment with TGF-β1 and CLU or not.