UBQLN4 promotes non-homologous end joining by repressing DNA end-resection

oleh: Ron D. Jachimowicz, H. Christian Reinhardt

Format: Article
Diterbitkan: Taylor & Francis Group 2019-03-01

Deskripsi

Ataxia-telangiectasia-mutated (ATM) promotes homologous recombination (HR)-mediated DNA double-strand break repair. It was recently shown that the proteasomal shuttle factor UBQLN4 facilitates MRE11 degradation to repress HR. Surprisingly, the UBQLN4-MRE11 interaction is ATM-dependent, suggesting that the proximal DNA damage kinase ATM does not only initiate HR, but also limits excessive end resection.