Integrating Myc and TGF-β signalling in cell-cycle control

Expression of the cell cycle inhibitor p15 INK4b is suppressed by the Myc oncoprotein and induced by transforming growth factor-β (TGF-β). The transcription factor Miz-1 activates the Ink4b promoter, and interacts with Myc and TGF-β-activated Smad proteins. Miz-1 is thus a point of convergence for t...

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Veröffentlicht in:	Nature cell biology 2001-05, Vol.3 (5), p.E112-E113
1. Verfasser:	Amati, Bruno
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biomedical and Life Sciences Cancer Research Carrier Proteins - genetics Carrier Proteins - metabolism Cell Biology Cell Cycle Cell Cycle Proteins Cyclin-Dependent Kinase Inhibitor p15 Cyclin-Dependent Kinase Inhibitor p16 Developmental Biology DNA-Binding Proteins - metabolism Gene expression Humans Kruppel-Like Transcription Factors Life Sciences Models, Biological news-and-views Physiological aspects Promoter Regions, Genetic Proto-Oncogene Proteins c-myc - metabolism Signal Transduction Smad3 Protein Smad4 Protein Stem Cells Trans-Activators - metabolism Transcription Factors Transcription, Genetic Transforming Growth Factor beta - metabolism Transforming growth factors Tumor Suppressor Proteins
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Zusammenfassung:	Expression of the cell cycle inhibitor p15 INK4b is suppressed by the Myc oncoprotein and induced by transforming growth factor-β (TGF-β). The transcription factor Miz-1 activates the Ink4b promoter, and interacts with Myc and TGF-β-activated Smad proteins. Miz-1 is thus a point of convergence for these antagonistic signals in cell-cycle control.
ISSN:	1465-7392 1476-4679
DOI:	10.1038/35074634