title: A protective role for BRCA2 at stalled replication forks.
abstract: The hereditary breast and ovarian cancer predisposition genes BRCA1 and BRCA2 account for the lion's share of heritable breast cancer risk in the human population. Loss of function of either gene results in defective homologous recombination (HR) and triggers genomic instability, accelerating breast tumorigenesis. A long-standing hypothesis proposes that BRCA1 and BRCA2 mediate HR following attempted replication across damaged DNA, ensuring error-free processing of the stalled replication fork. A recent paper describes a new replication fork protective function of BRCA2, which appears to collaborate with its HR function to suppress genomic instability.
authors: Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215, USA.
authors: Gurushankar
authors: G
authors: Chandramouly
authors: Nicholas A
authors: NA
authors: Willis
authors: Ralph
authors: R
authors: Scully
mesh_terms: D019313:BRCA1 Protein / Q000378:metabolism; D024682:BRCA2 Protein / Q000502:physiology*; D001943:Breast Neoplasms / Q000235:genetics*; D004261:DNA Replication / Q000187:drug effects; D005260:Female; D042822:Genomic Instability; D059765:Homologous Recombination; D006801:Humans; D006918:Hydroxyurea / Q000494:pharmacology; D009154:Mutation
chemical_list: D019313:BRCA1 Protein; C492913:BRCA1 protein, human; D024682:BRCA2 Protein; C551750:BRCA2 protein, human; D006918:Hydroxyurea