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. 2019 Jan 25;9:768. doi: 10.1038/s41598-018-36506-w

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Activation of the FA pathway after CRISPR/Cas9 templated repair in mouse ES cells. Western blot to detect short and long forms of FANCD2 in parental and template corrected mESCs. Upon exposure to hydroxy urea (HU) the short (S) from of FANCD2 becomes the long (L) form due to the ligation of a mono-ubiquitin group mediated by a functional FA core complex. The ESC corrected by Cas9D10A revealed one template repaired allele and one c.828InsTAAA allele, while the Cas9 WT ESC appeared homozygous for templated repair.