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.
Originalsprog | Engelsk |
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Tidsskrift | Nature Cell Biology |
Vol/bind | 17 |
Udgave nummer | 11 |
Sider (fra-til) | 1375-7 |
Antal sider | 3 |
ISSN | 1465-7392 |
DOI | |
Status | Udgivet - 1 nov. 2015 |