I am currently the postdoc research fellow in the Magnuson laboratory. I am interested in research on islet dysfunction in diabetes pathogenesis. My current research focuses on the function of rictor, which is the major component of mTORC2, in pancreatic islet β cell regeneration and dysfunction. Unlike mTORC1, mTORC2 is the upstream factor of AKT pathway, our hypothesis is that without rictor, AKT activity and then the regeneration of islet cells would be depressed. In addition, in the mouse model with constitutively stimulated AKT activity, like Pten knockout mice, loss of rictor would reverse the phenotype of islet hyperplasia.
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