The selective cancer killing properties of the homologous viral proteins apoptin and PCV1-VP3 may help reveal a novel target mechanism for cancer treatment. A difference between the two proteins is the subcellular localization behavior. It has been suggested that the cell-type specific nucleocytoplasmic shuttling of apoptin plays a role in selective induction of apoptosis by driving the protein into the nucleus of transformed cells. However, PCV1-VP3 does not display selective localization behavior, and remains in the cytoplasm while still causing cell death exclusively in cancer cells. This study employs both truncation and point mutants constructs to assess the functionality of nuclear export signal sequences predicted from the sequence of PCV1-VP3.
Worcester Polytechnic Institute
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Chemistry and Biochemistry
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