XRCC2 is Required for the Formation of Rad51 Foci Induced by Ionizing Radiation and DNA Cross-Linking Agent Mitomycin C.
XRCC2 is Required for the Formation of Rad51 Foci Induced by Ionizing Radiation and DNA Cross-Linking Agent Mitomycin C.
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XRCC2是由电离辐射和DNA交联丝霉素C诱导的RAD51焦点所必需的。
DOI：
10.1155/s1110724302204040
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发表时间：
2002
影响因子：
--
通讯作者：
Liu, Nan
中科院分区：
文献类型：
--
作者：
Liu, Nan
XRCC2蛋白与Rad51共享弱氨基酸序列相似性，Rad51是同源重组修复（HRR）的核心参与者。Rad51蛋白在HRR位点组装，并响应DNA损伤形成可见的核灶。Xrcc 2仓鼠突变irs1细胞不能形成Rad51灶后，电离辐射或DNA交联剂丝裂霉素C处理，虽然Rad51蛋白水平是正常的突变体。该缺陷可以在XRCC2扫描仪中得到纠正。时间进程研究表明，irs 1细胞主要缺乏形成小Rad51灶（1型）的早期反应（照射后2小时）和形成大灶（2型）的晚期反应（照射后8小时）。这些结果表明，XRCC2在DNA损伤诱导的Rad51灶的组装中是必需的，XRCC2可能在HRR的早期阶段起重要作用。
XRCC2 protein shares weak amino acid sequence similarity with Rad51, which is a central player in homologous recombinational repair (HRR). Rad51 proteins assemble at the sites of HRR and form visible nuclear foci in response to DNA damage. Xrcc2 hamster mutant irs1 cells are incapable of forming Rad51 foci after ionizing irradiation or DNA cross-linking agent mitomycin C treatment, though the Rad51 protein level is normal in the mutant. The defect can be corrected in an XRCC2 transformant. Time course study showed that the irs1 cells primarily lacked the early response (2 hours after irradiation) to form small Rad51 foci (type 1) and later response (8 hours after irradiation) to form large foci (type 2). These results suggested that XRCC2 is essential for the assembly of the DNA damage-induced Rad51 foci and that XRCC2 may play an important role in the early stage of HRR.