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

Delin Chen, Jing Shan, Wei-Guo Zhu, Jun Qin and Wei Gu ()
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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

Nature, 2010, vol. 464, issue 7288, 624-627

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.

Date: 2010
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DOI: 10.1038/nature08820

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