AI Article Synopsis
- Mazloum and Holloman (2009b) suggest that the collaboration between Rad51 and Brh2 facilitates 5' end strand invasion, which may help bypass DNA lesions during replication.
- This mechanism is linked to understanding the function of the BRCA2 tumor suppressor, which is crucial for maintaining genomic stability.
- Their findings could shed light on new strategies for addressing DNA repair processes in cancer research.
Article Abstract
In this issue of Molecular Cell, Mazloum and Holloman (2009b) propose that 5' end strand invasion promoted by collaboration between Rad51 and Brh2 could be used for bypassing lesions during DNA replication, potentially advancing understanding of BRCA2 tumor suppressor function.
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| http://dx.doi.org/10.1016/j.molcel.2009.11.003 | DOI Listing |
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