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  • Nbs1 is essential for DNA repair by homologous recombination in higher vertebrate cells [1].
  • The disruption of Nbs1 reduces gene conversion and sister chromatid exchanges, similar to other HR-deficient mutants [1].
  • Here, we show in vivo direct evidence that NBS1 recruits the hMRE11 nuclease complex into the cell nucleus and leads to the formation of foci by utilizing different functions from several domains [2].
  • The impairment of the HR pathway, which otherwise leads to cell death, may be somewhat substituted by an alternative mechanism such as the Mre11/Rad50/Nbs1 pathway, resulting in reduced frequencies of SCEs and CAs [3].

References

  1. Nbs1 is essential for DNA repair by homologous recombination in higher vertebrate cells. Tauchi, H., Kobayashi, J., Morishima, K., van Gent, D.C., Shiraishi, T., Verkaik, N.S., vanHeems, D., Ito, E., Nakamura, A., Sonoda, E., Takata, M., Takeda, S., Matsuura, S., Komatsu, K. Nature (2002) [Pubmed]
  2. The forkhead-associated domain of NBS1 is essential for nuclear foci formation after irradiation but not essential for hRAD50[middle dot]hMRE11[middle dot]NBS1 complex DNA repair activity. Tauchi, H., Kobayashi, J., Morishima, K., Matsuura, S., Nakamura, A., Shiraishi, T., Ito, E., Masnada, D., Delia, D., Komatsu, K. J. Biol. Chem. (2001) [Pubmed]
  3. Recombination repair pathway in the maintenance of chromosomal integrity against DNA interstrand crosslinks. Sasaki, M.S., Takata, M., Sonoda, E., Tachibana, A., Takeda, S. Cytogenet. Genome Res. (2004) [Pubmed]
 
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