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. Author manuscript; available in PMC: 2010 Aug 15.
Published in final edited form as: Eur J Pharmacol. 2009 Jun 17;616(1-3):31–37. doi: 10.1016/j.ejphar.2009.06.012

Fig. 4.

Fig. 4

NDGA inhibits Smad2 phosphorylation and transactivation mediated by TGF β type I receptor in cells. A. 293 FT cells were transfected with TGF β type I receptor T202D (receptor I T202D), a constitutively active mutant of TGF β type I receptor. Cells were treated with 40 µM NDGA or DMSO overnight. Phospho-Smad2 and Smad2 were by immunoblotting. Transfection of mutant receptor significantly increased Smad2 phosphorylation, and NDGA treatment inhibited this induction as well as the basal phosphorylation level of Smad2. There was no effect on total Smad2 level by any treatment. B. Panc-1 cells were transiently transfected with luciferase reporters CAGA12-Luc and pRL-null in the presence or absence of TGF β type I receptor T202D (receptor I T202D). Cells were treated with different amounts of NDGA overnight before being harvested for a luciferase assay. Transfection of mutant the receptor induced activation of the reporter, and NDGA repressed this activation in a dose-dependent manner.