Document Type
Journal Article
Publication Date
2016
Journal
Nucleic Acids Research
DOI
10.1093/nar/gkw1241
Abstract
Homologous recombination (HR) is a major mechanism to repair DNA double-strand breaks (DSBs). Although tumor suppressor CtIP is critical for DSB end resection, a key initial event of HR repair, the mechanism regulating the recruitment of CtIP to DSB sites remains largely unknown. Here, we show that acidic nucleoplasmic DNA‐binding protein 1 (And‐1) forms complexes with CtIP as well as other repair proteins, and is essential for HR repair by regulating DSB end resection. Furthermore, And-1 is recruited to DNA DSB sites in a manner dependent on MDC1, BRCA1 and ATM, down-regulation of And-1 impairs end resection by reducing the recruitment of CtIP to damage sites, and considerably reduces Chk1 activation and other damage response during HR repair. These findings collectively demonstrate a hitherto unknown role of MDC1→And-1→CtIP axis that regulates CtIP-mediated DNA end resection and cellular response to DSBs.
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
APA Citation
Li, Y., Li, Z., Han, Z., & Zhu, W. (2016). And-1 is required for homologous recombination repair by regulating DNA end resection. Nucleic Acids Research, (). http://dx.doi.org/10.1093/nar/gkw1241
Peer Reviewed
1
Open Access
1
Supplementary Data
Comments
Reproduced with permission of Oxford Journals. Nucleic Acids Research