作者: G NAGARAJU , R SCULLY
DOI: 10.1016/J.DNAREP.2007.02.020
关键词: RAD51 、 S phase 、 Biology 、 Genetics 、 DNA repair 、 Homologous recombination 、 DNA replication 、 Control of chromosome duplication 、 Eukaryotic DNA replication 、 Genome instability
摘要: The hereditary breast and ovarian cancer predisposition genes, BRCA1 BRCA2, participate in the repair of DNA double strand breaks by homologous recombination. Circumstantial evidence implicates these genes recombinational responses to polymerase stalling during S phase cell cycle. These play a key role preventing genomic instability cancer. Here, we review current literature implicating BRCA pathway HR at stalled replication forks explore hypothesis that BRCA2 resolution single stranded lesions termed "daughter gaps", generated across damaged template.