Jonah Kohen

P53 is a protein that supresses DNA replication and prevents excessive cell division. Mutations that suppress this protein's binding affinity have been implicated in more than 60% of all cancers. It has also been observed, however, that deactivated p53 can have functionality restored via the occurrence of another mutation. My research has two objectives: to determine how mutations to p53 alter its DNA binding site, and to learn how these observed "rescue mutations" alter the binding site in order to restore functionality. Through this I hope to create a reliable model that can accurately assess what mutations will restore p53 functionality.