It has previously been discovered that Apoptin has the ability to selectively kill cancer cells without affecting normal cells. This tumor-specific killing has made Apoptin a subject of much interest and speculation. On the structural level, Apoptin has Nuclear Localization Sequence (NLS) on the C-terminal end with Nuclear Export Sequence (NES) on the N-terminal end. Interestingly, the N-terminal NES overlaps with the domain for multimerization. Our study focuses on uncoupling the two domains in order to understand the role that each of them play to induce apoptosis in cancerous cells. The experiments focus on studying mutations in the overlapping domain in order to ablate one mechanism while retaining the other.
Worcester Polytechnic Institute
Major Qualifying Project
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Chemistry and Biochemistry
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