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Linking the p53 tumour suppressor pathway to somatic cell reprogramming

Author

Listed:
  • Teruhisa Kawamura

    (Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
    Career-Path Promotion Unit for Young Life Scientists, Kyoto University)

  • Jotaro Suzuki

    (Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
    Drug Discovery Research, Astellas Pharma Inc., Tsukuba, Ibaraki 305-8585, Japan)

  • 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
    Institució Catalana de Recerca i Estudis Avançats (ICREA), Passeig Lluis Companys 23
    Networking Center of Biomedical Research in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 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
    Center of Regenerative Medicine in Barcelona, Dr. Aiguader 88, 08003 Barcelona, Spain)

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.

Suggested Citation

  • Teruhisa Kawamura & Jotaro Suzuki & Yunyuan V. Wang & Sergio Menendez & Laura Batlle Morera & Angel Raya & Geoffrey M. Wahl & Juan Carlos Izpisúa Belmonte, 2009. "Linking the p53 tumour suppressor pathway to somatic cell reprogramming," Nature, Nature, vol. 460(7259), pages 1140-1144, August.
    • Handle: RePEc:nat:nature:v:460:y:2009:i:7259:d:10.1038_nature08311
    DOI: 10.1038/nature08311
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    Cited by:

    1. Siti Razila Abdul Razak & Kazuko Ueno & Naoya Takayama & Naoki Nariai & Masao Nagasaki & Rika Saito & Hideto Koso & Chen-Yi Lai & Miyako Murakami & Koichiro Tsuji & Tatsuo Michiue & Hiromitsu Nakauchi, 2013. "Profiling of MicroRNA in Human and Mouse ES and iPS Cells Reveals Overlapping but Distinct MicroRNA Expression Patterns," PLOS ONE, Public Library of Science, vol. 8(9), pages 1-16, September.
    2. 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.
    3. Tomoe Ueyama & Shu Nakao & Tasuku Tsukamoto & Dai Ihara & Yukihiro Harada & Yuka Akagi & Sae Nakagawa & Teruhisa Kawamura & Takahiro Sogo & Yasuyuki S Kida, 2018. "PTEN/Akt Axis is Involved in Somatic Cell Reprogramming to Mouse iPS Cells," Biomedical Journal of Scientific & Technical Research, Biomedical Research Network+, LLC, vol. 11(5), pages 8789-8795, December.

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