G-310 Health Sciences Building
My research is focused on defining novel molecular signaling mechanisms regulating cell growth and survival during physiological conditions and during cardiac hypertrophy and heart failure. We use genetically altered mice as model systems. We also use viral vector mediated gene transfer in cultured cardiomyocytes and other cell systems to investigate molecular signaling mechanisms underlying the cardiomyocyte hypertrophic growth and cell death. A better characterization of the signaling networks that control hypertrophy-specific gene expression will be paramount for designing novel therapeutic approaches with translational potential for heart failure.
We are particularly interested in elucidating novel cell signaling mechanisms in the heart involving protein kinases (e.g, PKC, ASK1, and TAK1) and phosphatases (e.g, PP1, PP2A, and calcineurin). Currently we are evaluating the role of TGFβ activated Kinase 1 (TAK1) as a central regulator of the hypertrophic signaling network in vivo using cardiac specific TAK1 transgenic and gene targeted mouse models. Our approach will suggest novel therapeutic strategies for the treatment of heart failure if conclusive proof is established in animal models. The laboratory is also interested in defining transcriptional regulatory mechanisms of cardiomyocyte growth and survival, with a focus on transcription factors NFAT and NFkB. Understanding of regulatory mechanisms of target gene expression will shed additional light on the regulatory paradigms that underlie cardiac hypertrophy and heart failure.
Copyright © 2003-2013 Molecular & Cellular Biology Program, University of Washington
Fred Hutchison Cancer Research Center | University of Washington
Institute for Systems Biology | Seattle Biomed