UV-induced ataxia-telangiectasia-mutated and Rad3-related (ATR) activation requires replication stress.

@article{Ward2004UVinducedAA,
  title={UV-induced ataxia-telangiectasia-mutated and Rad3-related (ATR) activation requires replication stress.},
  author={Irene M. Ward and Kay T Minn and Junjie Chen},
  journal={The Journal of biological chemistry},
  year={2004},
  volume={279 11},
  pages={9677-80}
}
Ataxia-telangiectasia-mutated and Rad3-related (ATR) plays an essential role in the maintenance of genome integrity and cell viability. The kinase is activated in response to DNA damage and initiates a checkpoint signaling cascade by phosphorylating a number of downstream substrates including Chk1. Unlike ataxia-telangiectasia-mutated (ATM), which appears to be mainly activated by DNA double-strand breaks, ATR can be activated by a variety of DNA damaging agents. However, it is still unclear… CONTINUE READING

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