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作 者:Ming Ma Fengfeng Zhuang Xiongbing Hu Bolun Wang Xian-Zi Wen Jia-Fu Ji Jianzhong Jeff Xi
机构地区:[1]Department of Biomedical Engineering, State Key Laboratory of Natural and Biomimetic Drugs, College of Engineering, Peking University, Beijing, China [2]Beijing Viewsolid Biotech Co. Ltd, Beijing 100071, China [3]Division of Gastrointestinal Cancer Translational Research Laboratory, Department of Gastrointestinal Surgery, Key Laboratory of Carcinogene- sis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, Fu-Cheng Road, Beijing, China [4]State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Molecular Medicine, Peking University, Beijing 100871, China [5]Collabo- rative Innovation Center for Cardiovascular Disorders, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China
出 处:《Cell Research》2017年第4期578-581,共4页细胞研究(英文版)
基 金:This research was supported by National Natural Science Foundation of China (NSFC; 81325010, 81421004 and 31371443) and Special Funding Support of Beijing Municipal Administration of Hospitals, Clinical Medicine Development (ZYLX201701).
摘 要:The clustered, regularly interspaced, short palin- dromic repeats (CRISPR)/CRISPR-associated protein 9 (Casg) system is a versatile tool for genomic engineering in mammalian cells and organisms, enabling the intro- duction of site-specific genomic double-strand breaks (DSBs) [1]. The resulting DSBs are repaired by at least two distinct and competitive mechanisms, nonhomolo- gous end-joining (NHEJ) and homology-directed repair (HDR). The former results in insertions and deletions (indels), whereas the latter leads to precise genetic modi- fication.
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