Nature Communications (Aug 2016)

Cullin3-KLHL15 ubiquitin ligase mediates CtIP protein turnover to fine-tune DNA-end resection

  • Lorenza P. Ferretti,
  • Sarah-Felicitas Himmels,
  • Anika Trenner,
  • Christina Walker,
  • Christine von Aesch,
  • Aline Eggenschwiler,
  • Olga Murina,
  • Radoslav I. Enchev,
  • Matthias Peter,
  • Raimundo Freire,
  • Antonio Porro,
  • Alessandro A. Sartori

DOI
https://doi.org/10.1038/ncomms12628
Journal volume & issue
Vol. 7, no. 1
pp. 1 – 16

Abstract

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CtIP has a key role in DNA double-strand break repair as its role in resecting DNA at the break commits a cell to homologous recombination. Here the authors show that KLHL15 interacts with CtIP and regulates repair by controlling protein turnover.