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Inhibition of 53BP1 favors homology-dependent DNA repair and increases CRISPR–Cas9 genome-editing efficiency
Nature Biotechnology ( IF 46.9 ) Pub Date : 2017-11-27 , DOI: 10.1038/nbt.4021
Marella D Canny,Nathalie Moatti,Leo C K Wan,Amélie Fradet-Turcotte,Danielle Krasner,Pedro A Mateos-Gomez,Michal Zimmermann,Alexandre Orthwein,Yu-Chi Juang,Wei Zhang,Sylvie M Noordermeer,Eduardo Seclen,Marcus D Wilson,Andrew Vorobyov,Meagan Munro,Andreas Ernst,Timothy F Ng,Tiffany Cho,Paula M Cannon,Sachdev S Sidhu,Frank Sicheri,Daniel Durocher

Inhibition of 53BP1 favors homology-dependent DNA repair and increases CRISPR–Cas9 genome-editing efficiency

Inhibition of 53BP1 favors homology-dependent DNA repair and increases CRISPR–Cas9 genome-editing efficiency, Published online: 27 November 2017; doi:10.1038/nbt.4021

Modulation of DNA repair pathway choice by a potent inhibitor of 53BP1 improves the efficiency of homology-dependent genome editing in human and mouse cells.


中文翻译:

抑制53BP1有助于同源性依赖性DNA修复,并提高CRISPR–Cas9基因组编辑效率

抑制53BP1有助于同源性依赖性DNA修复,并提高CRISPR–Cas9基因组编辑效率

抑制53BP1有利于同源性依赖性DNA修复,并提高CRISPR–Cas9基因组编辑效率,在线发布:2017年11月27日;doi:10.1038 / nbt.4021

通过有效的53BP1抑制剂调节DNA修复途径的选择,可提高人类和小鼠细胞中依赖同源基因组编辑的效率。
更新日期:2017-11-28
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