Multiple autophosphorylation sites are dispensable for murine ATM activation in vivo

@article{Daniel2008MultipleAS,
  title={Multiple autophosphorylation sites are dispensable for murine ATM activation in vivo},
  author={Jeremy A Daniel and Manuela Pellegrini and Ji-Hoon Lee and Tanya T Paull and L. Feigenbaum and Andr{\'e} Nussenzweig},
  journal={The Journal of Cell Biology},
  year={2008},
  volume={183},
  pages={777 - 783}
}
Cellular responses to both physiological and pathological DNA double-strand breaks are initiated through activation of the evolutionarily conserved ataxia telangiectasia mutated (ATM) kinase. Upon DNA damage, an activation mechanism involving autophosphorylation has been reported to allow ATM to phosphorylate downstream targets important for cell cycle checkpoints and DNA repair. In humans, serine residues 367, 1893, and 1981 have been shown to be autophosphorylation sites that are individually… CONTINUE READING
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Atm - defi cient mice : a paradigm of ataxia telangiectasia

  • R. J. Monnat
  • 2007

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