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Transcription-independent ARF regulation in oncogenic stress-mediated p53 responses

Author

Listed:
  • Delin Chen

    (Institute for Cancer Genetics, Columbia University, 1130 St Nicholas Avenue, New York, New York 10032, USA)

  • Jing Shan

    (Institute for Cancer Genetics, Columbia University, 1130 St Nicholas Avenue, New York, New York 10032, USA)

  • Wei-Guo Zhu

    (Peking University Health Science Center)

  • Jun Qin

    (Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA)

  • Wei Gu

    (Institute for Cancer Genetics, Columbia University, 1130 St Nicholas Avenue, New York, New York 10032, USA)

Abstract

ARF and p53 in oncogenic stress Of the known tumour suppressors, ARF and p53 are among the most relevant clinically, with p53 loss or inactivation found in more than half of human cancers and ARF known to activate p53 during oncogenic stress. A study of the mechanism of ARF-mediated p53 activation now shows that ARF is unstable in normal human cells but stable in cancer cells. In normal cells ARF ubiquitination and degradation is promoted by a ligase termed ULF (ubiquitin ligase for ARF), and this activity is abrogated in cancer cells.

Suggested Citation

  • Delin Chen & Jing Shan & Wei-Guo Zhu & Jun Qin & Wei Gu, 2010. "Transcription-independent ARF regulation in oncogenic stress-mediated p53 responses," Nature, Nature, vol. 464(7288), pages 624-627, March.
    • Handle: RePEc:nat:nature:v:464:y:2010:i:7288:d:10.1038_nature08820
    DOI: 10.1038/nature08820
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