title: BRCA2 function and the central nervous system.
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.
authors.affiliation: Department of Genetics and Tumor Cell Biology, St Jude Children's Research Hospital, Memphis, Tennessee, USA.
authors.forename: Pierre-Olivier
authors.initials: PO
authors.lastname: Frappart
authors.forename: Peter J
authors.initials: PJ
authors.lastname: McKinnon
mesh_terms: D000818:Animals; D024682:BRCA2 Protein / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D001921:Brain / Q000378:metabolism; D002490:Central Nervous System / Q000378:metabolism*; D004247:DNA / Q000235:genetics; D004249:DNA Damage / Q000235:genetics; D004260:DNA Repair / Q000235:genetics; D006801:Humans