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. 1998 Jul 15;12(14):2153–2163. doi: 10.1101/gad.12.14.2153

Figure 5.

Figure 5

Figure 5

 Model of Smad3/Smad4/CBP interactions at the promoter and inhibition of TGF-β- and Smad3/4-induced transcription by E1A. (A) A working model for TGF-β-inducible cooperation between Smad2/3, Smad4, and CBP/p300. Nuclear factor X is a hypothetical DNA-binding protein bound to the TGF-β-responsive elements, although Smad2/3 or Smad4 may directly bind to DNA. GTF represents a group of transcription factors for general transcription associated with RNA polymerase II. (B) E1A inhibits transcription from the PAI-1 promoter, induced by Smad3 and Smad4. Smad4-deficient SW480.7 cells were cotransfected with p800luc, and indicated combinations of expression plasmids for Smad3, Smad4, and E1A. (C) E1A, but not E1AΔ2–36, which is incapable of CBP association, inhibits TGF-β-induced transcription from the PAI-1 promoter. E1A928 has a point mutation at aa 928 and does not interact with pRB but still binds to CBP. Mv1Lu cells were cotransfected with p800luc, and wild-type or mutant E1A. (D) E1A, but not E1AΔ2–36, blocks TGF-β-induced transcription activity of GAL–Smad3 and the transactivation of GAL–Smad3 by CBP. Mv1Lu cells were cotransfected with pFR-Luc, and wild-type or mutant E1A, and CBP. (B–D) (Open bars) −TGF-β; (solid bars) +TGF-β.