A Protective Role for BRCA2 at Stalled Replication Forks
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CitationChandramouly, Gurushankar, Nicholas A. Willis, and Ralph Scully. 2011. A protective role for BRCA2 at stalled replication forks. Breast Cancer Research 13:314.
AbstractThe 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 longstanding 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.
Citable link to this pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:10026709
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