A prime editor mouse to model a broad spectrum of somatic mutations in vivo
T.J. is a member of the Board of Directors of Amgen and Thermo Fisher Scientific, and a co-founder of Dragonfly Therapeutics and T2 Biosystems. T.J. serves on the Scientific Advisory Board of Dragonfly Therapeutics, SQZ Biotech, and Skyhawk Therapeutics. T.J. is also the President of Break Through Cancer. None of these affiliations represent a conflict of interest with respect to the design or execution of this study or the interpretation of data presented in this manuscript.
Extended Data Fig. 2 Prime editing enables modeling a broader scope of cancer-associated mutations from residues conserved in mice at various homology stringencies.The percentage of mutations, categorized by variant type, that fall in a region of homology as a function of flank size. Flank size is defined as the number of amino acids on either side of the mutant codon that must match between the human and mouse orthologs for the mutated codon to be considered orthologous .
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