More Modifiers Move on DNA Damage

Research output: Contribution to journalArticle


Colleges, School and Institutes


In mammalian cells the accumulation of repair proteins to double-strand breaks is a phosphorylation- and ubiquitylation-regulated process. Some of the genes that encode the kinases and ubiquitin ligases in this pathway are cancer predisposition genes, most prominently the breast cancer predisposition gene BRCA1, which encodes a ubiquitin ligase. How BRCA1 ligase activity was regulated following DNA damage was poorly understood. In this review I summarize new data that show a third post-translational modification, by the small ubiquitin like modifier SUMO, is part of the same cascade, enabling and activating DNA damage-regulated processes, including the BRCA1 ligase activity.


Original languageEnglish
Pages (from-to)3861-3863
Number of pages3
JournalCancer Research
Issue number10
Publication statusPublished - 15 May 2010