作者: Ayako Nishihara , Jun-ichi Hanai , Nobuaki Okamoto , Jun Yanagisawa , Shigeaki Kato
DOI: 10.1046/J.1365-2443.1998.00217.X
关键词:
摘要: Background Smad proteins are novel transcriptional regulators mediating the signalling of transforming growth factor-β (TGF-β) superfamily. Coactivators such as p300/CBP promote transactivation by various transcription factors through a direct interaction with them. Adenoviral oncoprotein E1A, which binds p300, was shown to inhibit TGF-β. These findings raise possibility that p300 may be involved in TGF-β signalling. Results We investigated whether is Smads. enhanced Smad-induced p3TP-Lux, responsive reporter. E1A inhibited this enhancement, and inhibition required its ability bind p300/CBP. Smad3, well Smad2, interacted vivo ligand-dependent manner. The binding region Smad3 C-terminal half previously possess an intrinsic activity. mapped 678 amino acids. minimal Smad2/3-interacting region, rest p3TP-Lux dominant-negative fashion. Conclusion p300 Smad2 manner, Our results present molecular basis Smad proteins.