Loss of the ataxia-telangiectasia gene product causes oxidative damage in target organs.

@article{Barlow1999LossOT,
  title={Loss of the ataxia-telangiectasia gene product causes oxidative damage in target organs.},
  author={Carrolee Barlow and Phyllis A. Dennery and Mark K. Shigenaga and Mark A. Smith and Jason D. Morrow and L. Jackson Roberts and Anthony Wynshaw-Boris and Rodney L Levine},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={1999},
  volume={96 17},
  pages={9915-9}
}
Ataxia-telangiectasia (A-T) is characterized by a markedly increased sensitivity to ionizing radiation, increased incidence of cancer, and neurodegeneration, especially of the cerebellar Purkinje cells. Ionizing radiation oxidizes macromolecules and causes tissue damage through the generation of reactive oxygen species (ROS). We therefore hypothesized that A-T is due to oxidative damage resulting from loss of function of the A-T gene product. To assess this hypothesis, we employed an animal… CONTINUE READING

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