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J. Biol. Chem., Vol. 281, Issue 13, 99906, March 31, 2006

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Activation of a Tumor Suppressor

More than a decade after p53 was recognized as a major tumor suppressor, the p53 homolog p73 was identified. Like p53, p73 can induce cell cycle arrest and apoptosis in response to DNA damage or after the activation of selected oncogenes. However, p73 only activates the transcription of a subset of p53-responsive genes, and it interacts with different viral oncoproteins, indicating that despite their similarities, the two proteins have distinct cellular functions. Because of these differences it is important to understand the mechanisms that govern the regulation of both tumor suppressors.

p19ras co-localizes with p73.

Using the yeast two-hybrid screening method, Mi-Hee Jeong and colleagues have now identified a novel p73-binding protein. The protein, p19^ras, is an alternative splicing product of the proto-oncogene H-ras. When bound to p73, p19^ras stimulates its transcriptional activity. Jeong et al. also discovered that when p19^ras binds to MDM2, a known repressor of p73 and p53 transcriptional activity, it inhibits MDM2 association with p73 thereby abolishing MDM2-mediated transcriptional repression of p73. If p19^ras has a similar effect on p53, this would suggest that an alternatively spliced product of a prominent oncogene may activate tumor suppressor pathways, an important finding for the field of cancer biology.

FOOTNOTES

See referenced article, J. Biol. Chem. 2006, 281, 8707-8715

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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Related Collections Papers Of The Week Social Bookmarking                      What's this?