Abstract:
:Smad6 and Smad7 are inhibitory Smads induced by transforming growth factor beta-Smad signal transduction pathways in a negative-feedback mechanism. Previously it has been thought that inhibitory Smads bind to the type I receptor and block the phosphorylation of receptor-activated Smads, thereby inhibiting the initiation of Smad signaling. Conversely, few studies have suggested the possible nuclear functions of inhibitory Smads. Here, we present compelling evidence demonstrating that Smad6 repressed bone morphogenetic protein-induced Id1 transcription through recruiting transcriptional corepressor C-terminal binding protein (CtBP). A consensus CtBP-binding motif, PLDLS, was identified in the linker region of Smad6. Our findings show that mutation in the motif abolished the Smad6 binding to CtBP and subsequently its repressor activity of transcription. We conclude that the nuclear functions and physical interaction of Smad6 and CtBP provide a novel mechanism for the transcriptional regulation by inhibitory Smads.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Lin X,Liang YY,Sun B,Liang M,Shi Y,Brunicardi FC,Shi Y,Feng XHdoi
10.1128/mcb.23.24.9081-9093.2003subject
Has Abstractpub_date
2003-12-01 00:00:00pages
9081-93issue
24eissn
0270-7306issn
1098-5549journal_volume
23pub_type
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