Shorter telomeres, accelerated ageing and increased lymphoma in DNA-PKcs-deficient mice.

@article{Espejel2004ShorterTA,
  title={Shorter telomeres, accelerated ageing and increased lymphoma in DNA-PKcs-deficient mice.},
  author={Silvia Espejel and Marta L{\'o}pez Mart{\'i}n and Peter Klatt and Juan Mart{\'i}n-Caballero and Juana Mar{\'i}a Flores and Maria A Blasco},
  journal={EMBO reports},
  year={2004},
  volume={5 5},
  pages={503-9}
}
Non-homologous end joining (NHEJ) is the principal repair mechanism used by mammalian cells to cope with double-strand breaks (DSBs) that continually occur in the genome. One of the key components of the mammalian NHEJ machinery is the DNA-PK complex, formed by the Ku86/70 heterodimer and the DNA-PK catalytic subunit (DNA-PKcs). Here, we report on the detailed life-long follow-up of DNA-PKcs-defective mice. Apart from defining a role of DNA-PKcs in telomere length maintenance in the context of… CONTINUE READING

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