Atm selectively regulates distinct p53-dependent cell-cycle checkpoint and apoptotic pathways (original) (raw)

References

  1. Kastan, M.B. et al. A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia. Cell 71, 587–597 (1992).
    Article CAS PubMed Google Scholar
  2. Lu, X. & Lane, D.P. Differential induction of transcriptionally active p53 following UV or ionizing radiation: defects in chromosome instability syndromes? Cell 75, 765–778 (1993).
    Article CAS PubMed Google Scholar
  3. Khanna, K.K. & Lavin, M.F. Ionizing radiation and UV induction of p53 protein by different pathways in ataxia-telangiectasia cells. Oncogene 8, 3307–3312 (1993).
    CAS PubMed Google Scholar
  4. Xu, Y. & Baltimore, D. Dual responses of ATM in the cellular response to irradiation and in cell growth. Genes Dev. 10, 2401–2410 (1996).
    Article CAS PubMed Google Scholar
  5. Baskaran, R. et al. Ataxia telangiectasia mutant protein activates c-Abl tyrosine kinase in response to ionizing radiation. Nature 387, 516–519 (1997).
    Article CAS PubMed Google Scholar
  6. Ko, L.J. & Prives, C. p53: puzzle and paradigm. Genes Dev. 10, 1054–1072 (1996).
    Article CAS PubMed Google Scholar
  7. Levine, A.J. p53, the cellular gatekeeper for growth and division. Cell 88, 323–331 (1997).
    Article CAS PubMed Google Scholar
  8. Jacks, T. et al. Tumor spectrum analysis in p53-mutant mice. Curr. Biol. 4, 1–7 (1994).
    Article CAS PubMed Google Scholar
  9. Deng, C., Zhang, P., Harper, J.W., Elledge, S.J. & Leder, P. Mice lacking p21clp1/WAF1 undergo normal development, but are defective in G1 checkpoint control. Cell 82, 675–684 (1995).
    Article CAS PubMed Google Scholar
  10. Shiloh, Y. Ataxia-telangiectasia: closer to unraveling the mystery. Eur. J. Hum. Genet. 3, 116–38 (1995).
    Article CAS PubMed Google Scholar
  11. Meyn, M.S. Ataxia-telangiectasia and cellular responses to DNA damage. Cancer Res. 55, 5991–6001 (1995).
    CAS PubMed Google Scholar
  12. Barlow, C. et al. Atm-deficient mice: a paradigm of ataxia telangiectasia. Cell 86, 159–171 (1996).
    Article CAS PubMed Google Scholar
  13. Meyn, M.S., Strasfeld, L. & Alien, C. Testing the role of p53 in the expression of genetic instability and apoptosis in ataxia-telangiectasia. Int. J. Radiat. Biol. 66, 5141–5149 (1994).
    Article Google Scholar
  14. Westphal, C.H. et al atm and p53 cooperate in apoptosis and suppression of tumorigenesis, but not in resistance to acute radiation toxicity. Nature Genet. 16, 397–401 (1997).
    Article CAS PubMed Google Scholar
  15. Kastan, M.B., Onyekwere, O., Sidransky, D., Vogelstein, B. & Craig, R.W. Participation of p53 protein in the cellular response to DNA damage. Cancer Res. 51, 6304–6311 (1991).
    CAS PubMed Google Scholar
  16. Brugarolas, J. et al. Radiation-induced cell cycle arrest compromised by p21 deficiency. Nature 377, 552–557 (1995).
    Article CAS PubMed Google Scholar
  17. Lowe, S.W., Schmitt, E.M., Smith, S.W., Osborne, B.A. & Jacks, T. p53 is required for radiation-indiced apaptosis in mouse thymocytes. Nature 362, 847–849 (1993).
    Article CAS PubMed Google Scholar
  18. Clarke, A.R. et al. Thymocyte apoptosis induced by p53-dependent and independent pathways. Nature 362, 849–852 (1993).
    Article CAS PubMed Google Scholar
  19. Santana, P. et al. Acid sphingomyelinase-deficient human lymphoblasts and mice are defective in radiation-induced apoptosis. Cell 86, 189–199 (1996).
    Article CAS PubMed Google Scholar
  20. Chen, G. & Lee, E.Y.H.-P. The product of the ATM gene is a 370-kDa nuclear phosphoprotein. J.Biol. Chem. 271, 33693–33697 (1996).
    Article CAS PubMed Google Scholar
  21. Lakin, N.D. et al. Analysis of the ATM protein in wild-type and ataxia telangiectasia cells. Oncogene 13, 2707–2716 (1996).
    CAS PubMed Google Scholar
  22. Brown, K.D. et al. The ataxia-telangiectasia gene product, a constitutively expressed nuclear protein that is not upregulated following genome damage. Proc. Natl.Acad. Sci. USA 94, 1840–1845 (1997).
    Article CAS PubMed PubMed Central Google Scholar
  23. EI-Deiry, W.S. et al. WAF1, a potential mediator of p53 tumor suppression. Cell 75, 817–825 (1993).
    Article Google Scholar
  24. Harper, J.W., Adami, G.R., Wei, N., Keyomarsi, K. & Elledge, S.J. The p21 cdk-interacting protein Cip1 is a potent inhibitor of G1-cyclin-dependent kinases. Cell 75, 805–816 (1993).
    Article CAS PubMed Google Scholar
  25. Miyashita, T. & Reed, J.C. Tumor suppressor p53 is a direct transcriptional activator of the human bax gene. Cell 80, 293–299 (1995).
    Article CAS PubMed Google Scholar
  26. Friedlander, P., Haupt, Y., Prives, C. & Oren, M. A mutant p53 that discriminates between p53-responsive genes and cannot induce apoptosis.Mol. Cell. Biol. 16, 4961–4971 (1996).
    Article CAS PubMed PubMed Central Google Scholar
  27. Chen, X., Ko, L.J., Jayaraman, L. & Prives, C. p53 levels, functional domains, and DNA damage determine the extent of the apoptotic response of tumor cells. Genes Dev. 10, 2438–2451 (1996).
    Article CAS PubMed Google Scholar
  28. Pietenpol, J.A. et al. Sequence-specific transcriptional activation is essential for growth suppression by p53. Proc. Natl.Acad. Sci. USA 91, 1998–2002 (1994).
    Article CAS PubMed PubMed Central Google Scholar
  29. White, R.A., Terry, N.H., Meistrich, M.L. & Calkins, D.P. Improved method for computing potential doubling time from flow cytometric data. Cytometry 11, 314–317 (1990).
    Article CAS PubMed Google Scholar
  30. Luna, L.G. Methods and Color Atlas of Special Stainss and Tissue (American Histolabs, Gaithersburg, Maryland, 1992).
    Google Scholar
  31. Harlow, E. & Lane, D. Antibodies: A Laboratory Manual (Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, 1988).
    Google Scholar

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