期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 203, 期 13, 页码 2793-2799出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20061563
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资金
- Intramural NIH HHS Funding Source: Medline
The ataxia telangiectasia mutated (ATM) kinase is a key tumor suppressor that regulates numerous cell cycle checkpoints as well as apoptosis. Here, we report that ATM is a critical player in the regulation of apoptosis and lymphomagenesis in the presence of c-myc. In turn, deletion of the inhibitory ATM phosphatase, Wip1, results in ATM up-regulation and suppression of E mu-myc-induced B cell lymphomas. Using mouse genetic crosses, we show that the onset of myc-induced lymphomas is dramatically delayed in Wip1-null mice in an ATM- and p53-, but not p38 MAPK- or Arf-, dependent manner. We propose that Wip1 phosphatase is critical for regulating the ATM- mediated tumor surveillance network.
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