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1.National-Local Joint Engineering Research Center of Biodiagnosis & Biotherapy, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710004, China
2.The MOE Key Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou 310058, China
3.Zhejiang Provincial Key Lab of Geriatrics and Geriatrics Institute of Zhejiang Province, Department of Geriatrics, Zhejiang Hospital, Hangzhou 310030, China
4.Trauma Center, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
5.The Affiliated Hospital of Stomatology, School of Stomatology, Zhejiang University School of Medicine, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Hangzhou 310006, China
6.Zhejiang Provincial Key Laboratory of Cancer Molecular Cell Biology, Life Sciences Institute, Zhejiang University, Hangzhou 310058, China
7.Department of General Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310016, China
慕艳华,韩金花,邬明杰等.纤维蛋白通过促进重组酶RAD51在DNA损伤位点的招募参与同源重组修复[J].浙江大学学报(英文版)(B辑:生物医学和生物技术),2023,24(12):1165-1173.
Yanhua MU, Jinhua HAN, Mingjie WU, et al. Fibrillarin promotes homologous recombination repair by facilitating the recruitment of recombinase RAD51 to DNA damage sites. [J]. Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology) 24(12):1165-1173(2023)
慕艳华,韩金花,邬明杰等.纤维蛋白通过促进重组酶RAD51在DNA损伤位点的招募参与同源重组修复[J].浙江大学学报(英文版)(B辑:生物医学和生物技术),2023,24(12):1165-1173. DOI: 10.1631/jzus.B2300518.
Yanhua MU, Jinhua HAN, Mingjie WU, et al. Fibrillarin promotes homologous recombination repair by facilitating the recruitment of recombinase RAD51 to DNA damage sites. [J]. Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology) 24(12):1165-1173(2023) DOI: 10.1631/jzus.B2300518.
同源重组(HR)是一种高度精确的DNA双链断裂(DSB)损伤修复方式。HR修复的关键步骤是重组酶RAD51通过包裹单链DNA形成核酸蛋白纤维丝,进行同源模板搜索,并进行DNA链入侵反应,从而启动DNA修复合成。本研究发现,纤维蛋白(FBL)是重要的HR调节因子。一旦发生DNA损伤,FBL就被招募到DSB位点,并直接与RAD51互作。细胞缺失FBL会导致RAD51在DNA损伤位点募集减少,HR修复效率降低。此外,细胞缺失FBL会导致染色体畸变增加,促使细胞对DNA损伤药物敏感。本研究提出了FBL介导的RAD51在DNA损伤位点的招募的新机制,并强调了FBL在癌症治疗中的潜在意义。
基因组不稳定性DNA双链断裂同源重组RAD51纤维蛋白
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