抄録
DNA double-strand break (DSB), which is often induced by ionizing radiation, is the most serious damage in genome. There are at least two pathways which can repair DSBs: non-homologous end-joining (NHEJ) and homologous recombination (HR). When DSBs are generated by radiation, ATM kinase, which is activated by auto-phosphorylation and dissociation of their homodimer., phosphorylates histone H2AX. Subsequently, many repair proteins are recruited to the DSB sites and they activates damage responding pathways. A key role protein, Nbs1, physically interacts with phospho-H2AX for recruitment of a multi-functional repair complex, Mre11/Rad50/Nbs1, to DSB sites. This physical interaction requires the fork-head associated (FHA) domain of Nbs1 protein and the complex was found to be essential for HR. In this presentation, we will discuss about the processing and signaling pathways responding to radiation-induced DSBs. [J Radiat Res 44:375 (2003)]
