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作 者:Xiang Wei Fangfang Zhou Long Zhang
机构地区:[1]Life Sciences Institute,The Second Affiliated Hospital of the Zhejiang University School of Medicine,The MOE Key Laboratory of Biosystems Homeostasis&Protection and Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology,Zhejiang University,Hangzhou,China [2]The First Affiliated Hospital,the Institutes of Biology and Medical Sciences,Suzhou Medical College,Soochow University,Suzhou,Jiangsu 215123,China
出 处:《Signal Transduction and Targeted Therapy》2024年第6期2351-2353,共3页信号转导与靶向治疗(英文)
基 金:supported by Chinese National Natural Science Funds(31925013,32125016,U20A20393,T2321005);special programs from the Ministry of Science and Technology of China(2021YFA1101000 and 2023YFA1800200);Suzhou Innovation and Entrepreneurship Leading Talent Program(ZXL2022505,ZXL2022442);Priority Academic Program Development of Jiangsu Higher Education Institutions(PAPD).
摘 要:A recent study published by Simon Alberti1 in Cell has revealed that DNA double-strand break(DSB)sites that prevent the disjunction of broken DNA ends are formed through poly(ADPribose)(PAR)polymerase 1(PARP1)-DNA co-condensation.1(Fig.1).Here,a comprehensive and novel model was provided for the ordered assembly of PARP1-DNA condensates,which can rationally make clear broken DNA end synapses and how repair effectors are recruited to repair DSB.
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