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. 2016 Feb 27;23:30. doi: 10.1186/s12929-016-0229-4

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© Chen et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 4 — BetA enhances TGF-β-induced Smad2 phosphorylation and nuclear translocation in Mv1Lu cells. Cells were pretreated with BetA, for 0, 0.5, 1, 2, 4, and 6 h, and then further incubated with 100 pM TGF-β for 30 min. The P-Smad2 and total Smad2 levels in the cell lysates were analyzed by immunoblotting. The relative level of P-Smad2 (P-Smad2/Smad2) was estimated. A representation of 2 analyses is shown (a). The quantitative analysis of the immunoblots is shown (b). The relative level of P-Smad2 in cells treated only with TGF-β was taken as 100 % of TGF-β-stimulated Smad2 phosphorylation. The data from three different analyses represents the mean ± SD. **Significantly higher than that in cells treated with TGF-β alone (P < 0.01)