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. 2021 Jan 21;22(3):1046. doi: 10.3390/ijms22031046

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Western blot analysis of TGFbeta-1-induced phosphorylation of Smad2 protein in glioma cells. (A) U87 glioma cells and (B) AZVU001A glioma stem-like cells treated with recombinant TGFbeta-1 for the indicated times showed the presence of phosphorylated Smad2 (pSmad2) protein (lanes 5, 6, and 7, upper immunoblots). pSmad2 was undetectable in U87 glioma cells and in AZVU001A glioma stem-like cells cultured in the absence of TGFbeta-1 (lanes 2, 3, and 4, upper immunoblots) or in the presence of both TGFbeta-1 and TGFbeta type I receptor inhibitor A7701 (lanes 8, 9, and 10, upper immunoblots). The lower immunoblots show immunodetection of GAPDH which served as a protein loading control.