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

Crossref DOI link: https://doi.org/10.1038/nbt.4021

Published Online: 2017-11-27

Published Print: 2018-01

Update policy: https://doi.org/10.1007/springer_crossmark_policy

Authors

Canny, Marella D

Moatti, Nathalie

Wan, Leo C K

Fradet-Turcotte, Amélie

Krasner, Danielle

Mateos-Gomez, Pedro A

Zimmermann, Michal

Orthwein, Alexandre

Juang, Yu-Chi

Zhang, Wei

Noordermeer, Sylvie M https://orcid.org/0000-0003-2737-9690
Seclen, Eduardo

Wilson, Marcus D

Vorobyov, Andrew

Munro, Meagan

Ernst, Andreas

Ng, Timothy F

Cho, Tiffany

Cannon, Paula M

Sidhu, Sachdev S

Sicheri, Frank

Durocher, Daniel https://orcid.org/0000-0003-3863-8635
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Article History

Received: 28 March 2016

Accepted: 20 October 2017

First Online: 27 November 2017

Change Date: 14 December 2017

Change Type: Corrigendum

Change Details: In the version of this article initially published, the affiliation footnotes of Andrew Vorobyov and Sachdev S Sidhu were erroneously given as number 4, the Skirball Institute of Biomolecular Medicine, instead of number 5, The Donnelly Centre for Cellular and Biomolecular Research. The errors have been corrected for the print, PDF and HTML versions of this article.

Competing interests

: The use of 53BP1-blocking Ubvs for stimulating genome editing are the subject of a patent application and a license agreement.