Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. STKE, 26 October 1999
Vol. 1999, Issue 5, p. tw6
[DOI: 10.1126/stke.1999.5.tw6]

EDITORS' CHOICE

Cell proliferation Cell proliferation: Interfering with Smads

Unregulated cell growth results in tumor production; therefore, it is important to identify developmental factors that regulate cell growth. Transforming growth factor-beta (TGF-β) regulates cell growth and differentiation through receptor-mediated phosphorylation of Smad proteins. These Smad proteins in turn form protein complexes and enter the cell's nucleus to activate the transcription of target genes. Stroschein et al. have identified a new player, SnoN, in TGF-β signaling. In the absence of TGF-β, the SnoN oncoprotein binds to a Smad2/Smad4 complex and recruits a transcription co-repressor, thus inhibiting transcription activation. When TGF-β is present, Smad3 triggers the degradation of SnoN and transcription activation resumes. Finally, a negative-feedback mechanism is present in which TGF-β stimulates SnoN production, which then represses the transcription activation function of the Smad complex once again. SnoN is found in various carcinomas. Hence, the transforming activity of SnoN may be explained by its interference with the role of TGF-β in inhibiting cell growth.

Stroschein, S.L., Wang, W., Zhou, S., Zhou, Q., and Luo, K. (1999) Negative feedback regulation of TGF-signaling by the SnoN oncoprotein. Science 286: 771 - 774. [Abstract] [Full Text]

Citation: Cell proliferation: Interfering with Smads. Sci. STKE 1999, tw6 (1999).


To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882