Linking the p53 tumour suppressor pathway to somatic cell reprogramming

Teruhisa Kawamura, Jotaro Suzuki, Yunyuan V. Wang, Sergio Menendez, Laura Batlle Morera, Angel Raya, Geoffrey M. Wahl () and Juan Carlos Izpisúa Belmonte ()
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Teruhisa Kawamura: Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
Jotaro Suzuki: Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
Yunyuan V. Wang: Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
Sergio Menendez: Center of Regenerative Medicine in Barcelona, Dr. Aiguader 88, 08003 Barcelona, Spain
Laura Batlle Morera: Center of Regenerative Medicine in Barcelona, Dr. Aiguader 88, 08003 Barcelona, Spain
Angel Raya: Center of Regenerative Medicine in Barcelona, Dr. Aiguader 88, 08003 Barcelona, Spain
Geoffrey M. Wahl: Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
Juan Carlos Izpisúa Belmonte: Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA

Nature, 2009, vol. 460, issue 7259, 1140-1144

Abstract: On iPS cells and p53: somatic cell reprogramming This paper reports that the transcription factor p53 plays a crucial role in regulating somatic reprogramming. The authors develop an experimental protocol to reprogram somatic cells using just two factors, Oct4 and Sox2, when p53 is silenced. On the other hand, overexpression of p53 or the presence of Nutlin-3 (a p53 stabilizer) reduces reprogramming efficiency.

Date: 2009
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DOI: 10.1038/nature08311

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