| Literature DB >> 17786054 |
Pierre-Olivier Frappart1, Peter J McKinnon.
Abstract
Defective responses to DNA double strand breaks (DSBs) in the nervous system can lead to neurodegeneration or tumorigenesis. A key player in the repair of DNA DSBs is the tumor suppressor BRCA2, an essential component of the homologous recombination repair pathway and the Fanconi Anemia complex. We recently demonstrated that BRCA2 was required for normal neurogenesis and prevention of medulloblastoma brain tumors. Here, we discuss how this study contributes both to our understanding of BRCA2 functions in vivo, and the tissue-specific requirements for DNA repair and damage-signaling pathways.Entities:
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Year: 2007 PMID: 17786054 DOI: 10.4161/cc.6.20.4785
Source DB: PubMed Journal: Cell Cycle ISSN: 1551-4005 Impact factor: 4.534