Complexity in signaling networks is often derived from co-opting one set of molecules for multiple operations. Understanding how cells achieve such sophisticated processing using a finite set of molecules within a confined space--what we call the "signaling paradox"--is critical to biology and engineering as well as the emerging field of synthetic biology.
In the Inoue Lab, we have recently developed a series of chemical-molecular tools that allow for inducible, quick-onset and specific perturbation of various signaling molecules. Using this novel technique in conjunction with fluorescence imaging, microfabricated devices, quantitative analysis and computational modeling, we are dissecting intricate signaling networks.
In particular, we investigate positive-feedback mechanisms underlying the initiation of neutrophil chemotaxis (known as symmetry breaking), as well as spatio-temporally compartmentalized signaling of Ras and membrane lipids such as phosphoinositides. In parallel,... we also try to understand how cell morphology affects biochemical pathways inside cells. Ultimately, we will generate completely orthogonal machinery in cells to achieve existing, as well as novel, cellular functions. Our synthetic, multidisciplinary approach will elucidate the signaling paradox created by nature.view more
Research in the Peter Abadir Lab focuses on the renin-angiotensin system (RAS), a signaling pathway that regulates blood pressure and has been linked independently to both aging and inflammation. We’re particularly interested in changes in RAS that occur with aging. We also study signal transduction and the role of the crosstalk between angiotensin II receptor in aging and are interested in understanding the function of angiotensin II in the process of vascular aging.
The Jia lab performs basic and translational research into the mechanisms of and therapeutic strategy for viral and bacterial infection-induced inflammatory lung diseases, one of the leading causes of death in pulmonary diseases, especially for the ongoing pandemic of the SARS-CoV-2 mediated COVID-19. Our work has identified novel roles of Angiotensin-converting enzyme 2 (ACE2) in the inflammatory response to viral and bacterial lung infection and its complex contributions into the pathogenesis and disease progression and outcome of COVID-19. In seeking to translate these findings to clinical studies, we have been working on a collaboration with other investigators, developing novel diagnostic, preventive, and therapeutic tools in combating the devastating COVID-19, even in the era of effective vaccine prevention. These studies are funded by NIAID.