Dr. Ito graduated with a B. Sc. in Biochemistry from the University of Tokyo in 1979 and earned a M. Sc (Biochemistry) from the University of Tokyo in 1981. He obtained his Ph.D. (Biochemistry) at the Institute of Medical Science at University of Tokyo in 1984.
He did his postdoctoral studies in the field of human interferon signal transduction in Dr. Peter Lengyel's lab at Yale University from 1985-1988. He then moved to California and worked in Dr. Atsushi Miyajima's lab in DNAX Research Institute in Palo Alto, California. In Dr. Miyajima's lab, he and others cloned the human Interleukin-3 receptor using an antibody as a probe using "Panning method" developed by Dr. Brian Seed. This was one of the first human interleukin receptors cloned and had contributed to the better understanding of the signal transduction pathway by cytokine receptors in immune system. After spending two years in California, he became a senior scientist in the Osaka Bioscience Institute in Osaka, Japan in 1990. There, he cloned the human Fas antigen receptor (CD95) gene in Dr. Shigekazu Nagata's group. This was the first death receptor cloned and Dr. Nagata and Dr. Ito established the notion that death is regulated from outside of the cells by ligand-receptor system. They also determined the domain required for death-signal transduction in Fas antigen cytoplasmic region ("death domain").
During his work on the signal transduction mechanism of cytokine receptor system and death receptor system, Dr. Ito realized the importance of genetic approach to understand the signal transduction system, and had decided to go to Dr. Gerry Rubin's lab at University of California at Berkeley in 1993 to learn genetical analysis using Drosophila. In Dr. Rubin's lab, he joined a group conducting an extensive genetic screen to identify mutants that affect the eye development. He cloned one of the genes whose loss-of-function mutation produced larger cell size (gigas), and found that gigas gene encodes a fly homolog of Tuberous Sclerosis gene-2 (TSC2). He also identified a fly homolog of another human Tuberous Sclerosis gene, TSC1. This work has opened up a new wave of research in fly and human that have established that TSC1 and TSC2 gene products negatively regulate cell growth by inhibiting an Insulin receptor signaling pathway. This approach has provided new insights how TSC genes normally work and already provided some information that may give ways to develop drugs that will lessen the symptoms in human Tuberous Sclerosis Complex (TSC) patients.
Dr. Ito is currently working with Dr. Jim Gusella to establish and study fly models of human neurological diseases, (TSC, Dystonia and Huntington). They are trying to isolate mutants of fly genes and will study their functions in Drosophila. They are also trying to identify other genes that interact with these human disease gene orthologs. Since Drosophila and human share most of the genes and molecular machineries, we are hoping that we can learn a lot about human genes by studying fly counterparts.
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