Skip to main content
. Author manuscript; available in PMC: 2010 Aug 24.
Published in final edited form as: Mol Cancer Res. 2008 May;6(5):695–705. doi: 10.1158/1541-7786.MCR-07-0294

FIGURE 2.

FIGURE 2

TGF-β1, TGF-β2, and TGF-β3 stimulate Smad3 phosphorylation and nuclear localization. OVCA429 cells were made quiescent and then treated with vehicle, 10 ng/mL TGF-β1, TGF-β2, or TGF-β3. A. Anti–phosphorylated Smad3 immunoblot. OVCA429 cells were treated with TGF-β ligands for 0, 10, 20, 30, 45, and 60 min. The same blot was stripped and reprobed with anti-Smad3 as a loading control. B. Anti–phosphorylated Smad2 immunoblot. OVCA429 cells were treated with TGF-β ligands for 0, 10, 20, 30, 45, and 60 min. The same blot was reprobed with anti-Smad2 as a loading control. Lysates from LβT2 cells treated with activin A were used as a control for anti–phosphorylated Smad2 immunoreactivity. C. Fluorescent micrograph of cells transfected with Smad3-GFP for 24 h before treatment with vehicle, TGF-β1, TGF-β2, or TGF-β3 for 30 min. Bar, 50 μm.