Abstract

Two studies show that the E3 ubiquitin ligase RNF138 is recruited to DNA double-strand break sites, where it ubiquitylates key repair factors to promote DNA-end resection and homologous recombination. These findings add insights into the multilayered regulatory mechanisms underlying DNA double-strand break repair pathway choice in mammalian cells.

OriginalsprogEngelsk
TidsskriftNature Cell Biology
Vol/bind17
Udgave nummer11
Sider (fra-til)1375-7
Antal sider3
ISSN1465-7392
DOI
StatusUdgivet - 1 nov. 2015

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