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. Author manuscript; available in PMC: 2013 Aug 8.
Published in final edited form as: J Biol Chem. 2004 Dec 3;280(9):8079–8085. doi: 10.1074/jbc.M409647200

Figure 2. Deletion of AP-1 binding site abolishes UV stimulation of Smad7 promoter activity.

Figure 2

Human skin fibroblasts were transiently transfected with wild-type Smad7 promoter/luciferase construct (-613 to +112) containing Smad3 element (SBE) and AP-1 element (AP-1E), or constructs with SBE or AP-1E deleted (depicted in the figure). Cells were co-transfected with β-galactosidase expression vector. Cells were irradiated with UV (50 mJ/cm2) 24 hours after transfection, and cell lysates were prepared 24 hours post UV. Smad7 promoter/luciferase activities were normalized to β-galactosidase activity. Bars indicate means ± SEM fold change in Smad7 promoter activity relative to non-irradiated, wild-type Smad7 control cells. *p<0.05 vs. non-irradiated, wild-type Smad7 control cells. N=3.