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. 2020 Mar 31;11(3):211. doi: 10.1038/s41419-020-2404-5

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© The Author(s) 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. 2 — a, b Real-time PCR and western blotting and analyses showed the expression of CTR1 in NRK-49F cells after the simultaneous knockdown of Smad2 and Smad3 and treatment as indicated (n = 5). c, d Binding protein prediction in the rat CTR1 promoters using two evolutionarily conserved predicted binding sites (http://ecrbrowser.dcode.org/ and http://jaspardev.genereg.net/) for Smad3. Note that the NRK-49F cell line used in this study originated in rats. e Chromatin immunoprecipitation (ChIP) assay followed by PCR showed that Smad3 physically binds to the CTR1 promoter in response to TGF-β1 after 24 h (n = 5). Data represent the mean ± SEM. **P < 0.01 versus blank control cells. #P < 0.05 versus TGF-β1-treated cells.