作者: Kyoko Nakamura , Wataru Sakai , Takuo Kawamoto , Ronan T. Bree , Noel F. Lowndes
DOI: 10.1016/J.DNAREP.2006.03.008
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摘要: Abstract 53BP1 (p53 binding protein) is a BRCT domain-containing protein that rapidly recruited to DNA double strand breaks (DSBs). To investigate the role of in damage response, we generated 53BP1−/− cells from chicken DT40 cell line. As mammalian cells, mutation increased cellular sensitivity ionizing radiation. Although depletion resulted checkpoint defects had normal intra S phase and G2/M checkpoints. G1 specific radiosensitivity higher topoisomerase II suggested defective non-homologous end joining (NHEJ) cells. Genetic analyses confirm this suggestion as have demonstrated an epistatic relationship between NHEJ genes, Ku70 Artemis, but not with Rad54, gene essential for repair DSBs by homologous recombination. We conclude major supporting survival suffered facilitating NHEJ.