Interaction between ATM protein and c-Abl in response to DNA damage

  title={Interaction between ATM protein and c-Abl in response to DNA damage},
  author={T. Shafman and K. Khanna and P. Kedar and K. Spring and S. Kozlov and T. Yen and K. Hobson and M. Gatei and N. Zhang and D. Watters and M. Egerton and Y. Shiloh and S. Kharbanda and D. Kufe and Martin F. Laving},
  • T. Shafman, K. Khanna, +12 authors Martin F. Laving
  • Published 1997
  • Biology, Medicine
  • Nature
  • The gene mutated in the autosomal recessive disorder ataxia telangiectasia (AT), designated ATM (for 'AT mutated'), is a member of a family of phosphatidylinositol-3-kinase-like enzymes that are involved in cell-cycle control, meiotic recombination, telomere length monitoring and DNA-damage response1–4. Previous results have demonstrated that AT cells are hypersensitive to ionizing radiation5–7 and are defective at the Gl/S checkpoint after radiation damage8–10. Because cells lacking the… CONTINUE READING
    475 Citations
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    ATM: from gene to function.
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    Nature of G1/S cell cycle checkpoint defect in ataxia-telangiectasia.
    • 99
    Role for c-Abl tyrosine kinase in growth arrest response to DNA damage
    • 232
    The stress response to ionizing radiation involoves c-Abl-dependent phosphorylation of SHPTP1.
    • S. Kharbanda, A. Bharti, +6 authors D. Kufe
    • Biology, Medicine
    • Proceedings of the National Academy of Sciences of the United States of America
    • 1996
    • 94
    • PDF