Research Paper Volume 16, Issue 7 pp 6588—6612
TGF-β downstream of Smad3 and MAPK signaling antagonistically regulate the viability and partial epithelial–mesenchymal transition of liver progenitor cells
Figure 7. TGF-β downstream of MAPK signaling promotes linker phosphorylation of Smad3 in liver progenitor cells. (A) Schematic representation of the phosphorylation sites in Smad2 and Smad3. (B) WB-F344 and LE/6 cells were treated with TGF-β (10 ng/ml) for the indicated times, and lysates were subjected to Western blot analyses with antibodies against the indicated phospho- and total Smad proteins. GAPDH was used as a loading control. (C–E) WB-F344 and LE/6 cells were treated with TGF-β (10 ng/ml, 1 h) and/or kinase inhibitors as indicated for 1 h or 3 h, and Western blot analyses were carried out with antibodies against the indicated phospho- and total Smad proteins. GAPDH was used as a loading control. The experiments were repeated three times, and representative images are shown.