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Gene Review

ATM  -  ataxia telangiectasia mutated

Gallus gallus

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Disease relevance of ATM


High impact information on ATM

  • These results suggest that ATM has multiple p53-independent functions in cell cycle checkpoint control and in maintenance of chromosomal DNA [2].
  • To further define the physiological roles of ATM at the cellular level, we created an isogenic set of stable cell lines differing only in their ATM status from the chicken B cell line DT40 by targeted integration [2].
  • ATM is a member of the large phosphatidylinositol-3 kinase family and plays an important role in cellular response to DNA damage [2].
  • We further found that Rad17-/- and Rad9-/- but not ATM-/- cells are defective in S-phase DNA damage checkpoint controls and in the cellular response to stalled DNA replication [3].
  • We found that ATM(-/-) DT40 cells were more susceptible than wild-type cells to apoptosis induced not only by ionizing radiation and bleomycin but also by non-DNA-damaging apoptotic stimuli such as C(2)-ceramide [1].

Biological context of ATM


Associations of ATM with chemical compounds

  • Furthermore, the apoptosis induced by C(2)-ceramide and H(2)O(2) was blocked by anti-oxidants, indicating that the ATM(-/-) DT40 cells had a heightened susceptibility to apoptosis induced by reactive oxygen intermediates (ROI), presumably due to defective ROI-detoxification activities [1].
  • We show that caffeine efficiently abolishes S- and G(2)-phase checkpoint responses after irradiation in all cell lines tested and greatly radiosensitizes wild-type and ATM(-/-) cells, the partially checkpoint-deficient cells [5].
  • BLM(-/-) cells showed sensitivity to methyl methanesulfonate (MMS) and UV irradiation while ATM(-/-) cells did not show sensitivity to either agent [4].

Other interactions of ATM

  • Disrupting the function of ATM reduced the targeted integration frequency in BLM(-/-) DT40 cells [4].


  1. Protective roles for ATM in cellular response to oxidative stress. Takao, N., Li, Y., Yamamoto, K. FEBS Lett. (2000) [Pubmed]
  2. Disruption of ATM in p53-null cells causes multiple functional abnormalities in cellular response to ionizing radiation. Takao, N., Kato, H., Mori, R., Morrison, C., Sonada, E., Sun, X., Shimizu, H., Yoshioka, K., Takeda, S., Yamamoto, K. Oncogene (1999) [Pubmed]
  3. Critical role for chicken Rad17 and Rad9 in the cellular response to DNA damage and stalled DNA replication. Kobayashi, M., Hirano, A., Kumano, T., Xiang, S.L., Mihara, K., Haseda, Y., Matsui, O., Shimizu, H., Yamamoto, K. Genes Cells (2004) [Pubmed]
  4. The absence of a functional relationship between ATM and BLM, the components of BASC, in DT40 cells. Wang, W., Seki, M., Otsuki, M., Tada, S., Takao, N., Yamamoto, K., Hayashi, M., Honma, M., Enomoto, T. Biochim. Biophys. Acta (2004) [Pubmed]
  5. Caffeine could not efficiently sensitize homologous recombination repair-deficient cells to ionizing radiation-induced killing. Wang, H., Wang, X., Iliakis, G., Wang, Y. Radiat. Res. (2003) [Pubmed]
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