Journal
NATURE MEDICINE
Volume 24, Issue 7, Pages 927-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41591-018-0049-z
Keywords
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Funding
- Science for Life Laboratory (Scilifelab)
- Knut and Alice Wallenberg Foundation
- Cancerfonden
- Barncancerfonden
- Academy of Finland
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Here, we report that genome editing by CRISPR-Cas9 induces a p53-mediated DNA damage response and cell cycle arrest in immortalized human retinal pigment epithelial cells, leading to a selection against cells with a functional p53 pathway. Inhibition of p53 prevents the damage response and increases the rate of homologous recombination from a donor template. These results suggest that p53 inhibition may improve the efficiency of genome editing of untransformed cells and that p53 function should be monitored when developing cell-based therapies utilizing CRISPR-Cas9.
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