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Sci. Signal., 1 June 2010
Vol. 3, Issue 124, p. ra44
[DOI: 10.1126/scisignal.2000758]


Editor's Summary

Time and Tools for Repair
ATM is a kinase activated in response to DNA damage, such as that caused by exposure of cells to ionizing radiation. ATM triggers cell cycle checkpoints that allow cells time to repair the damage before proceeding to replicate their DNA. With reversible inhibitors, White et al. show that ATM and DNA-PK, another kinase induced by DNA damage, initiated distinct mechanisms of DNA repair in cells exposed to ionizing radiation. Despite activation of the cell cycle checkpoint, cells in which either of these two kinases was inhibited for as little as 1 hour 15 min after exposure to ionizing radiation exhibited reduced survival and accumulated persistent chromosomal damage. Furthermore, the authors show that ATM-deficient cells adapt and can initiate repair by sister chromatid exchange through an ATM-independent mechanism.

Citation: J. S. White, S. Choi, C. J. Bakkenist, Transient ATM Kinase Inhibition Disrupts DNA Damage–Induced Sister Chromatid Exchange. Sci. Signal. 3, ra44 (2010).

Read the Full Text

ATR kinase activation in G1 phase facilitates the repair of ionizing radiation-induced DNA damage.
A. M. Gamper, R. Rofougaran, S. C. Watkins, J. S. Greenberger, J. H. Beumer, and C. J. Bakkenist (2013)
Nucleic Acids Res. 41, 10334-10344
   Abstract »    Full Text »    PDF »
ATM Kinase Inhibition Preferentially Sensitizes p53-Mutant Glioma to Ionizing Radiation.
L. Biddlestone-Thorpe, M. Sajjad, E. Rosenberg, J. M. Beckta, N. C. K. Valerie, M. Tokarz, B. R. Adams, A. F. Wagner, A. Khalil, D. Gilfor, et al. (2013)
Clin. Cancer Res. 19, 3189-3200
   Abstract »    Full Text »    PDF »
Double-strand break repair by homologous recombination in primary mouse somatic cells requires BRCA1 but not the ATM kinase.
E. M. Kass, H. R. Helgadottir, C.-C. Chen, M. Barbera, R. Wang, U. K. Westermark, T. Ludwig, M. E. Moynahan, and M. Jasin (2013)
PNAS 110, 5564-5569
   Abstract »    Full Text »    PDF »
Human Papillomavirus Episome Stability Is Reduced by Aphidicolin and Controlled by DNA Damage Response Pathways.
T. G. Edwards, M. J. Helmus, K. Koeller, J. K. Bashkin, and C. Fisher (2013)
J. Virol. 87, 3979-3989
   Abstract »    Full Text »    PDF »
Ataxia Telangiectasia Mutated (ATM) Is Dispensable for Endonuclease I-SceI-induced Homologous Recombination in Mouse Embryonic Stem Cells.
E. Rass, G. Chandramouly, S. Zha, F. W. Alt, and A. Xie (2013)
J. Biol. Chem. 288, 7086-7095
   Abstract »    Full Text »    PDF »
Kinase-dead ATM protein causes genomic instability and early embryonic lethality in mice.
K. Yamamoto, Y. Wang, W. Jiang, X. Liu, R. L. Dubois, C.-S. Lin, T. Ludwig, C. J. Bakkenist, and S. Zha (2012)
J. Cell Biol. 198, 305-313
   Abstract »    Full Text »    PDF »
Homologous chromosomes make contact at the sites of double-strand breaks in genes in somatic G0/G1-phase human cells.
M. Gandhi, V. N. Evdokimova, K. T.Cuenco, M. N. Nikiforova, L. M. Kelly, J. R. Stringer, C. J. Bakkenist, and Y. E. Nikiforov (2012)
PNAS 109, 9454-9459
   Abstract »    Full Text »    PDF »
ATM Protein Physically and Functionally Interacts with Proliferating Cell Nuclear Antigen to Regulate DNA Synthesis.
A. M. Gamper, S. Choi, Y. Matsumoto, D. Banerjee, A. E. Tomkinson, and C. J. Bakkenist (2012)
J. Biol. Chem. 287, 12445-12454
   Abstract »    Full Text »    PDF »
Functional characterization connects individual patient mutations in ataxia telangiectasia mutated (ATM) with dysfunction of specific DNA double-strand break-repair signaling pathways.
M. Keimling, M. Volcic, A. Csernok, B. Wieland, T. Dork, and L. Wiesmuller (2011)
FASEB J 25, 3849-3860
   Abstract »    Full Text »    PDF »
The Genomics of Lung Adenocarcinoma: Opportunities for Targeted Therapies.
H. Greulich (2010)
Genes & Cancer 1, 1200-1210
   Abstract »    Full Text »    PDF »

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