Genomic evolvability endows viruses and tumor cells the abilities to accrue drug resistance mutations that ultimately defeat therapeutic regimens. The APOBEC family of single-stranded DNA cytosine-to-uracil deaminases are endogenous enzymes that contribute to the mutational load of both virus and cancer genomes. Therefore, inhibition of APOBEC-catalyzed deamination may slow or prevent the development of drug resistance mutations. Our team has identified small molecule and nucleic acid probes for APOBEC enzymes, as well as proteins essential for APOBEC expression and function, using a powerful discovery strategy that integrates experimental and computational approaches. This presentation, which will be coordinated with computational collaborator Prof. Rommie Amaro (University of California, San Diego), will focus on the experimental aspects of our work.

Development of chemical probes to explore APOBEC-catalyzed mutation: An integrated experimental and computational approach

2019 Fall National Meeting

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