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研究领域

Cells interpret and respond to environmental cues using a signaling network comprising chemical and physical interactions between molecules that, ultimately, modulate cellular behavior. During viral infection, these signaling networks are "hijacked" and rewired by virus proteins in order to induce a state of viral pathogenesis. Dr. Miller-Jensen’s group applies quantitative, systems-level approaches to study signaling aspects of viral infection and develop novel anti-viral therapies. Her lab uses genetically-engineered viruses to study viral infection, as well as experimental and computational techniques for monitoring changes in the signaling network induced by these infections. She is currently interested in studying how proteins expressed in early-stage HIV infections establish a pathogenic state in cells of the immune system, and how latent HIV can be reactivated to purge chronic infections.

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Burnett, J.C., Miller-Jensen, K., Shah, P.S., Arkin, A.P., Schaffer, D.V (2009). Control of stochastic gene expression by host factors at the HIV promoter, PLoS Pathogens, 5(1): e1000260. Miller-Jensen, K.*, Janes, K.A.*, Brugge, J. S., Lauffenburger, D.A. (2007). Common effector processing mediates cell-specific responses to stimuli, Nature, 448, 604-8. (Research highlight in Nature Biotechnology, 9/07) Miller-Jensen, K., Janes, K.A., Wong, Y., Griffith, L.G., Lauffenburger, D.A. (2006). Adenoviral vector saturates Akt pro-survival signaling and blocks insulin-mediated rescue of tumor necrosis-factor-induced apoptosis, J Cell Science, 119, 3788-98.

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