14-3-3σ controls mitotic translation to facilitate cytokinesis

Erik W. Wilker, Marcel A. T. M. van Vugt, Stephen C. Artim, Paul H. Huang, Christian P. Petersen, H. Christian Reinhardt, Yun Feng, Phillip A. Sharp, Nahum Sonenberg, Forest M. White and Michael B. Yaffe ()
Additional contact information
Erik W. Wilker: Center for Cancer Research
Marcel A. T. M. van Vugt: Center for Cancer Research
Stephen C. Artim: Center for Cancer Research
Paul H. Huang: Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
Christian P. Petersen: Center for Cancer Research
H. Christian Reinhardt: Center for Cancer Research
Yun Feng: Center for Cancer Research
Phillip A. Sharp: Center for Cancer Research
Nahum Sonenberg: McGill Cancer Centre, McGill University, Montreal, Quebec, H3G 1Y6, Canada
Forest M. White: Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
Michael B. Yaffe: Center for Cancer Research

Nature, 2007, vol. 446, issue 7133, 329-332

Abstract: A translational switch The protein known as 14-3-3σ is an important p53-regulated human tumour suppressor that is lost early in cancer development. A possible molecular basis for its function has now been found. While mRNA translation normally switches from a 'cap-dependent' to 'cap-independent' mechanism during mitosis, cells lacking 14-3-3σ don't make this switch, and consequently have cell division abnormalities.

Date: 2007
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DOI: 10.1038/nature05584

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