期刊
NUCLEIC ACIDS RESEARCH
卷 43, 期 2, 页码 987-999出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gku1384
关键词
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资金
- Spanish Ministry of Economy and Competitivity [SAF2010-14877]
- European Research Council (ERC) Starting Grant [DSBRECA]
- ERC Starting Grant [DSBRECA]
DNA double strand breaks are the most cytotoxic lesions that can occur on the DNA. They can be repaired by different mechanisms and optimal survival requires a tight control between them. Here we uncover protein deneddylation as a major controller of repair pathway choice. Neddylation inhibition changes the normal repair profile toward an increase on homologous recombination. Indeed, RNF111/UBE2M-mediated neddylation acts as an inhibitor of BRCA1 and CtIP-mediated DNA end resection, a key process in repair pathway choice. By controlling the length of ssDNA produced during DNA resection, protein neddylation not only affects the choice between NHEJ and homologous recombination but also controls the balance between different recombination subpathways. Thus, protein neddylation status has a great impact in the way cells respond to DNA breaks.
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