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Targeting Repair Pathways With Small Molecules Increases Precise Genome Editing In Pluripotent Stem Cells
A now frequently used method to edit mammalian genomes uses the nucleases CRISPR/Cas9 and CRISPR/Cpf1 or the nickase CRISPR/Cas9n to introduce double-strand breaks (DSBs) which are then repaired by homology-directed repair (HDR) using synthetic or cloned DNA donor molecules carrying desired mutations. However, another pathway, the non-homologous end joining (NHEJ) pathway competes with HDR for repairing DNA breaks in cells. To increase the frequency of precise genome editing in human induceddoi:10.1101/136374 fatcat:44g52uk3trhedgmyjyt3jpwkw4