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. 2016 Nov 28;16(4):319–334. doi: 10.1080/15384101.2016.1259037

Figure 3.

Figure 3.

OSM/STAT3 signaling promotes SMAD3 nuclear localization without increased phosphorylation. (A) Western analysis of whole cell lysates harvested from shp53-HMEC plated in the presence (+) and absence (-) of either OSM or TGF-β1 for 4 and 8 d. (B) Western analysis of the nuclear-soluble protein fractions from subcellular fractionations of untreated shp53-HMEC and shp53-HMEC treated with either OSM or TGF-β1 for 4 d. (C) Western analysis of SMAD3-specific immunoprecipitations using whole cell lysates from both untreated and OSM-treated HEK 293T cells transfected with an expression vector encoding SMAD3 in combination with either an expression vector encoding wild-type STAT3 (WT-STAT3) or encoding dominant-negative STAT3 (DN-STAT3), and then plated in the presence (+) and absence (-) of recombinant OSM [10 ng/mL] for 2 d.