Negative Feedback Regulation of TGF-β Signaling by the SnoN Oncoprotein

descriptionPublicationkeyboard_double_arrow_right Article 22 Oct 1999 English Publisher:American Association for the Advancement of Science (AAAS)Journal:Science, volume 286, pages 771-774 (issn: 0036-8075, eissn: 1095-9203,

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Authors: S L, Stroschein; W, Wang; S, Zhou; Q, Zhou; K, Luo;

doi: 10.1126/science.286.5440.771

pmid: 10531062

Negative Feedback Regulation of TGF-β Signaling by the SnoN Oncoprotein

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Abstract

Smad proteins mediate transforming growth factor–β (TGF-β) signaling to regulate cell growth and differentiation. The SnoN oncoprotein was found to interact with Smad2 and Smad4 and to repress their abilities to activate transcription through recruitment of the transcriptional corepressor N-CoR. Immediately after TGF-β stimulation, SnoN is rapidly degraded by the nuclear accumulation of Smad3, allowing the activation of TGF-β target genes. By 2 hours, TGF-β induces a marked increase in SnoN expression, resulting in termination of Smad-mediated transactivation. Thus, SnoN maintains the repressed state of TGF-β–responsive genes in the absence of ligand and participates in negative feedback regulation of TGF-β signaling.

Related Organizations

Lawrence Berkeley National Laboratory
United States
University of California, Berkeley
United States
Direction de la Recherche Fondamentale
France

Keywords

Cell Nucleus, Intracellular Signaling Peptides and Proteins, Nuclear Proteins, DNA, Smad2 Protein, Cell Line, Feedback, DNA-Binding Proteins, Repressor Proteins, Gene Expression Regulation, Proto-Oncogene Proteins, Trans-Activators, Humans, Nuclear Receptor Co-Repressor 1, Smad3 Protein, Promoter Regions, Genetic, Cell Division, Signal Transduction, Smad4 Protein, Transcription Factors

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