Matrin3 promotes homologous recombinational repair by regulation of RAD51.
Matrin3 promotes homologous recombinational repair by regulation of RAD51.
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DOI：
10.1093/jb/mvz041
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发表时间：
2019-05
影响因子：
2.7
通讯作者：
Lin Shi;Jiying Sun;A. Kinomura;Atsuhiko Fukuto;Yasunori Horikoshi;S. Tashiro
中科院分区：
文献类型：
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作者：
Lin Shi;Jiying Sun;A. Kinomura;Atsuhiko Fukuto;Yasunori Horikoshi;S. Tashiro
Matrin3是一种高度保守的内核基质蛋白，参与RNA代谢的多个阶段。虽然Matrin3也可能在DNA修复中发挥作用，但其确切作用仍不清楚。在本研究中，我们发现Matrin3的缺失导致同源重组（HR）效率降低和细胞辐射敏感性增加。Matrin3缺失的细胞表现出受损的DNA损伤依赖性焦点形成的RAD51，HR中的一个关键蛋白。这些研究结果表明，Matrin3通过调节RAD51促进HR。
Matrin3 is a highly conserved inner nuclear matrix protein involved in multiple stages of RNA metabolism. Although Matrin3 may also play a role in DNA repair, its precise roles have remained unclear. In the present study, we showed that the depletion of Matrin3 led to decreased homologous recombination (HR) efficiency and increased radiation sensitivity of cells. Matrin3-depleted cells showed impaired DNA damage-dependent focus formation of RAD51, a key protein in HR. These findings suggest that Matrin3 promotes HR by regulating RAD51.