Ataxia telangiectasia mutated expression and activation in the testis.

@article{Hamer2004AtaxiaTM,
  title={Ataxia telangiectasia mutated expression and activation in the testis.},
  author={Geert Hamer and Henk B. Kal and Christoph H. Westphal and T Clay Ashley and Dirk G de Rooij},
  journal={Biology of reproduction},
  year={2004},
  volume={70 4},
  pages={
          1206-12
        }
}
Ionizing radiation (IR) and consequent induction of DNA double-strand breaks (DSBs) causes activation of the protein ataxia telangiectasia mutated (ATM). Normally, ATM is present as inactive dimers; however, in response to DSBs, the ATM dimer partners cross-phosphorylate each other on serine 1981, and kinase active ATM monomers are subsequently released. We have studied the presence of both nonphosphorylated as well as active serine 1981 phosphorylated ATM (pS1981-ATM) in the mouse testis. In… CONTINUE READING
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