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PTPRV is a Key Mediator of p53-Induced Cell Cycle Exit
Gilles Doumont, Alain Martoriati and Jean-Christophe Marine
volume 4 | issue 12
december 2005Pages: 1703 - 1705
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The p53 tumor suppressor functions as a sequence-specific DNA-binding transcription factor that promotes antiproliferative responses, including cell cycle checkpoints, cellular senescence and apoptosis. The precise nature of the p53 transcriptional programs and the complex mechanisms that govern whether or not a cell dies in response to p53 activation remain elusive. We have recently reported the identification of a new direct p53 target, Ptprv, encoding a transmembrane tyrosine phosphatase. Ptprv expression is dramatically and preferentially increased in cells undergoing p53-dependent cell cycle exit, but not in cells undergoing p53-mediated apoptosis. Importantly, while p53-induced apoptosis is intact in mice lacking Ptprv, Ptprv-null cells are defective in G1 checkpoint control. In addition, we report herein that Ptprv is induced at high cell density and mediates contact inhibition of cell growth. Together, the data suggest that Ptprv is a potent inhibitor of cell proliferation and a critical mediator of p53-induced cell cycle exit.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.