atm and p53 cooperate in apoptosis and suppression of tumorigenesis, but not in resistance to acute radiation toxicity

@article{Westphal1997atmAP,
  title={atm and p53 cooperate in apoptosis and suppression of tumorigenesis, but not in resistance to acute radiation toxicity},
  author={Christoph H. Westphal and Sheldon Rowan and Cornelius Schmaltz and Ari Elson and David E Fisher and Philip Leder},
  journal={Nature Genetics},
  year={1997},
  volume={16},
  pages={397-401}
}
  • Christoph H. Westphal, Sheldon Rowan, +3 authors Philip Leder
  • Published 1997
  • Biology, Medicine
  • Nature Genetics
  • Mutations in atm and p53 cause the human cancer-associated diseases ataxia-telangiectasia1 and Li-Fraumeni syndrome2,3, respectively. The two genes are believed to interact in a number of pathways4–6, including regulation of DNA damage–induced cell-cycle checkpoints7, apoptosis and radiation sensitivity8, and cellular proliferation9. Atm-null mice10–12, as well as those null for p5313,14, develop mainly T-cell lymphomas, supporting the view that these genes have similar roles in thymocyte… CONTINUE READING

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