Immortalization eliminates a roadblock during cellular reprogramming into iPS cells

Jochen Utikal, Jose M. Polo, Matthias Stadtfeld, Nimet Maherali, Warakorn Kulalert, Ryan M. Walsh, Adam Khalil, James G. Rheinwald and Konrad Hochedlinger ()
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Jochen Utikal: Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, Harvard Stem Cell Institute, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Jose M. Polo: Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, Harvard Stem Cell Institute, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Matthias Stadtfeld: Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, Harvard Stem Cell Institute, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Nimet Maherali: Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, Harvard Stem Cell Institute, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Warakorn Kulalert: Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, Harvard Stem Cell Institute, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Ryan M. Walsh: Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, Harvard Stem Cell Institute, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Adam Khalil: Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, Harvard Stem Cell Institute, 185 Cambridge Street, Boston, Massachusetts 02114, USA
James G. Rheinwald: Brigham and Women’s Hospital and Harvard Skin Disease Research Center, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA
Konrad Hochedlinger: Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, Harvard Stem Cell Institute, 185 Cambridge Street, Boston, Massachusetts 02114, USA

Nature, 2009, vol. 460, issue 7259, 1145-1148

Abstract: On iPS cells and p53: removing the roadblock Pluripotency can be induced in somatic cells by overexpression of a set of transcription factors. The process has extremely low efficiency and slow kinetics. Here Utikal et al. show that cells with low endogenous p19Arf levels and immortal fibroblasts deficient for components of the Ink4a/Arf/p53 pathway yield iPS colonies with a threefold faster kinetics and at a significantly higher efficiency compared with wild-type cells, reaching frequencies of up to 100%. Genetic deletion of p53 in cellular subpopulations that normally fail to reprogram rescues their ability to produce iPS cells.

Date: 2009
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DOI: 10.1038/nature08285

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