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A missense mutation of Smad2 identified in cancer cells was reconstructed on the corresponding residue of Smad3. This mutant, Smad3D407E, was not phosphorylated by the constitutively active form of type I receptor for transforming growth factor-β (TGF-β), and inhibited the phosphorylation of co-expressed wild-type Smad2 and Smad3. This mutant also had a dominant negative effect on the growth inhibition...
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