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UBQLN4 promotes non-homologous end joining by repressing DNA end-resection
oleh: Ron D. Jachimowicz, H. Christian Reinhardt
Format: | Article |
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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.