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. Author manuscript; available in PMC: 2014 Nov 15.
Published in final edited form as: Exp Cell Res. 2013 Sep 27;319(19):2928–2937. doi: 10.1016/j.yexcr.2013.07.013

Figure 5. Role of the Serine-204 (S204) Smad3LR Phosphorylation Site in Smad3-mediated renal epithelial cell COL1A2 promoter activity.

Figure 5

A, Effect of the S204A-Smad3 mutant on Smad3-mediated COL1A2 promoter activity in renal epithelial cells. Smad3-knockdown HKC (bars 1–6) and Smad3-null MEFs (bars 7–12) were transfected with empty vector or pCS2-Smad3 constructs (wild-type or S204A), including the COL1A2-luciferase and β-galactosidase constructs for 3 hours. The transfected cells were then stimulated with TGF-β (2 ng/ml) for a further 20 h. Relative luciferase activity (mean ± S.E.M., n=3) was corrected for β-galactosidase activity. Shown here is a representative experiment of three independent experiments. *P<0.05, **P<0.01 vs. vehicle-treated cells. B, Smad3-knockdown in renal epithelial cells. Western blotting analysis of HKC stably expressing control- or Smad3-pGIPZ lentiviral shRNA.