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B.S., University of Utah, Salt Lake City, UT, 2011
Honors and Awards:
The APOBEC3 family of cytidine deaminases is exploited during the innate immune response to repress infections by deaminating viral single stranded DNA. However, recent work has shown that APOBEC3 enzymes can become misregulated and contribute to cancer mutagenesis. One family member in particular, A3B (APOBEC3B), causes mutations in many cancer types. A3B is not expressed in normal tissues but becomes upregulated in malignant tissues as well as virally infected cells. Thus, A3B is beneficial by suppressing viral infection, but its misregulation can cause collateral damage to the host genome. Using a combination of molecular and genetic approaches, my goal is to elucidate the mechanism through which A3B gains access to the host genome and ultimately how A3B activity is regulated.