Abstract: The p53 gene acts as a tumor suppressor by inducing growth arrest or apoptosis during the cell cycle. Mutations of p53 are responsible for about half of all human cancers. Extensive research has been done on the resulting protein and, more specifically, the protein’s DNA binding domain. Humans have nine isoforms of p53: the full-length wildtype, and eight splice variants that contain portions of the tails. Most existing studies focus exclusively on the wildtype and its DNA binding domain, often leaving out the tails of the wildtype and the eight other isoforms. My research serves to explore the behavior of the full-length wildtype p53 and its isoforms to learn about their potential regulatory effects.
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