| Citation | Vice President and Chief Scientific Officer, Howard Hughes Medical Institute and Professor of Pharmacology, Cell & Molecular Medicine, Chemistry and Biochemistry, University of California, San Diego
Jack E. Dixon is one of the most influential biochemists of his generation. His elegant studies have radically advanced our understanding of cell signaling and the molecular basis of pathogenesis. He was instrumental in the analysis of protein tyrosine phosphatases (PTPases). His pioneering work on the catalytic mechanism of PTPases showed that they function via a novel cysteine-phosphate intermediate. Dixon also discovered that the bacterium responsible for the plague or "black death", Yersinia pestis, harbors the most active PTPase yet described. This enzyme functions as a "lethal weapon when "injected" into mammalian cells to block the immune response. This mechanism is now recognized as a widely used strategy for pathogenic bacteria to disarm the host's immune system. Dixon's interest in phosphatases led to analysis of the tumor suppressor protein, PTEN, which shares sequence identity with the PTPases. He showed that PTEN dephosphorylates a lipid (PIP3). Loss of PTEN elevates PIP3 levels causing cells to survive and become oncogenic. Dixon is a powerful advocate for scientific research; a member of the National Academy of Sciences USA, a past president of the American Society for Biochemistry and Molecular Biology, and Vice President and Chief Scientific Officer at Howard Hughes Medical Institute.
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