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. 2021 Mar;31(3):461–471. doi: 10.1101/gr.265736.120

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© 2021 Bosch-Guiteras et al.; Published by Cold Spring Harbor Laboratory Press

This article, published in Genome Research, is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 3. — DNA-PKcs inhibition boosts CRISPR-del independent of cell, readout, or sgRNA delivery method. (A) CRISPR-del efficiency of CiDER in HeLa upon DNA ligase 4 inhibition (mean). (B) CiDER measurement of CRISPR-del efficiency in HCT116 and HEK293T cell lines upon DNA-PKcs inhibition (mean, standard deviation, one-tailed paired t-test). (C) CRISPR-del efficiency at MALAT1-enhancer upon DNA-PKcs inhibition. (Left) The fraction of WT allele quantified by qPCR (mean, standard deviation, one-tailed paired t-test). (Center) The pgRNAs, PCR primers, and a representative agarose gel from the genomic PCR of the region. (Right) Quantification of the KO band from the gel. (D) CRISPR-del efficiency of CiDER in HeLa as a result of initiating DNA-PKcs inhibition at 24 h after lentiviral infection (MOI = 0.3).