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Suppression of induced pluripotent stem cell generation by the p53–p21 pathway

Author

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  • Hyenjong Hong

    (Center for iPS Cell Research and Application (CiRA), Institute for Integrated Cell-Material Sciences, Kyoto University
    Institute for Frontier Medical Sciences, Kyoto University)

  • Kazutoshi Takahashi

    (Center for iPS Cell Research and Application (CiRA), Institute for Integrated Cell-Material Sciences, Kyoto University)

  • Tomoko Ichisaka

    (Center for iPS Cell Research and Application (CiRA), Institute for Integrated Cell-Material Sciences, Kyoto University
    Yamanaka iPS Cell Special Project, Japan Science and Technology Agency)

  • Takashi Aoi

    (Center for iPS Cell Research and Application (CiRA), Institute for Integrated Cell-Material Sciences, Kyoto University)

  • Osami Kanagawa

    (Laboratory for Autoimmune Regulation, RIKEN Center for Allergy and Immunology, RIKEN Yokohama Institute, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan)

  • Masato Nakagawa

    (Center for iPS Cell Research and Application (CiRA), Institute for Integrated Cell-Material Sciences, Kyoto University
    Institute for Frontier Medical Sciences, Kyoto University)

  • Keisuke Okita

    (Center for iPS Cell Research and Application (CiRA), Institute for Integrated Cell-Material Sciences, Kyoto University)

  • Shinya Yamanaka

    (Center for iPS Cell Research and Application (CiRA), Institute for Integrated Cell-Material Sciences, Kyoto University
    Institute for Frontier Medical Sciences, Kyoto University
    Yamanaka iPS Cell Special Project, Japan Science and Technology Agency
    Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA)

Abstract

On iPS cells and p53: role of p53–p21 pathway Induced pluripotent stem (iPS) cells are generated from mouse and human somatic cells by introduction of four genes. Efficiency of this process, however, is low. Here it is reported that up to 10% of transduced mouse embryonic fibroblasts (MEF) lacking p53 became iPS cells, even without the Myc retrovirus. In the p53-null background, iPS cells can be generated from terminally differentiated T lymphocytes. The authors propose that the p53–p21 pathway serves as a barrier not only in tumorigenicity, but also in iPS cell generation.

Suggested Citation

  • Hyenjong Hong & Kazutoshi Takahashi & Tomoko Ichisaka & Takashi Aoi & Osami Kanagawa & Masato Nakagawa & Keisuke Okita & Shinya Yamanaka, 2009. "Suppression of induced pluripotent stem cell generation by the p53–p21 pathway," Nature, Nature, vol. 460(7259), pages 1132-1135, August.
    • Handle: RePEc:nat:nature:v:460:y:2009:i:7259:d:10.1038_nature08235
    DOI: 10.1038/nature08235
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    Cited by:

    1. Daniel F. Kaemena & Masahito Yoshihara & Meryam Beniazza & James Ashmore & Suling Zhao & Mårten Bertenstam & Victor Olariu & Shintaro Katayama & Keisuke Okita & Simon R. Tomlinson & Kosuke Yusa & Keis, 2023. "B1 SINE-binding ZFP266 impedes mouse iPSC generation through suppression of chromatin opening mediated by reprogramming factors," Nature Communications, Nature, vol. 14(1), pages 1-16, December.
    2. Mu Li & Aaron Zhong & Youjun Wu & Mega Sidharta & Michael Beaury & Xiaolan Zhao & Lorenz Studer & Ting Zhou, 2022. "Transient inhibition of p53 enhances prime editing and cytosine base-editing efficiencies in human pluripotent stem cells," Nature Communications, Nature, vol. 13(1), pages 1-12, December.
    3. Ali Doğa Yücel & Vadim N. Gladyshev, 2024. "The long and winding road of reprogramming-induced rejuvenation," Nature Communications, Nature, vol. 15(1), pages 1-9, December.

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