Author: Zhao, Bing; Chen, Ye-Guang
Title: Regulation of TGF-ß Signal Transduction Document date: 2014_9_23
ID: 1ag9mnd2_22
Snippet: In addition, we reported that in some cell lines, including Hep3B, HeLa, L17 cells (a mutant mink lung epithelial Mv1Lu cell line lacking T RI) and human normal lung epithelial HPL-1 cells, Smad7 is predominantly localized in the nucleus and can inhibit the transcriptional activity of the functional R-Smad-Smad4 complex, independently, of inhibition of the type I receptors [99] . Unlike R-Smads and Smad4, which bind to DNA through their MH1 domai.....
Document: In addition, we reported that in some cell lines, including Hep3B, HeLa, L17 cells (a mutant mink lung epithelial Mv1Lu cell line lacking T RI) and human normal lung epithelial HPL-1 cells, Smad7 is predominantly localized in the nucleus and can inhibit the transcriptional activity of the functional R-Smad-Smad4 complex, independently, of inhibition of the type I receptors [99] . Unlike R-Smads and Smad4, which bind to DNA through their MH1 domains, biotinylated oligonucleotide pull-down assays and single-molecule force spectroscopy studies showed that Smad7 binds to DNA through its MH2 domain and thus represses TGF-signaling by interfering with the functional R-Smads/Smad4-DNA complex formation on the target gene promoters [99, 100] (Figure 4(b) ). These results suggest that Smad7 can inhibit TGF-signaling in the nucleus by a novel mechanism.
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