Hiroshi Senoo
G-protein-coupled receptors (GPCRs) activate mTORC2-AKT signaling in metabolism, cell survival and cytoskeleton dynamics. Altered mTORC2-AKT signaling leads to many human diseases, including cancer, metastasis and metabolic syndromes; however, it is unknown how mTORC2 is activated downstream of GPCRs. Using proteomic approaches, I identified a GDP-bound RhoGTPase as an mTORC2-binding protein and identified its function in mTORC2-AKT signaling by reconstituting GPCR-mediated mTORC2-AKT activation with purified mTORC2, Rho and Ras.
My discoveries rewrite the central dogma that G proteins are only active in a GTP-bound state and further our understanding of mTORC2-AKT-related human diseases.
Questions & Answers
Why did you choose Johns Hopkins for your work?
Because Miho Iijima, who is my mentor, is one of the fabulous scientist in the cell migration field.
What does receiving this award mean to you personally and professionally? Do you have any connection with the particular award you received?
I’m delighted to announce this award to the Japanese government because they gave me a chance and fellowship.
What contributed to your project’s success? (Special skills, interests, opportunities, guidance, etc.)
Discussion with my mentors, Miho Iijima and Hiromi Sesaki as well as fellowship from the Japanese government.
What has been your best/most memorable experience while at Johns Hopkins?
When I found a novel mechanism by which mTORC2-AKT signaling is activated by Rho-GDP, it was the most memorable result for me.
Tell us something interesting about yourself.
My unique set of expertise in cell biology, molecular biology and biochemistry allows me to conduct unparalleled research in the field of biomedical life science.