Kirk M. Druey, M.D.
Chief, Molecular Signal Transduction Section
Senior Investigator
Dr. Druey obtained his M.D. from Rush Medical College in Chicago, IL. In 1992, following a residency in internal medicine at The New York Hospital/Cornell Medical Center, Dr. Druey became a postdoctoral fellow in the NIAID Laboratory of Immunoregulation. He joined the Laboratory of Allergic Diseases in 1997 to become Chief of the Molecular Signal Transduction Section (MSTS).
Description of Research Program
The primary focus of our laboratory is to understand the signaling pathways evoked by G-protein-coupled receptors (GPCRs) and the role of specific GPCRs in the pathogenesis of asthma and other allergic diseases. Although therapeutic agents targeting GPCRs have long been used to treat asthma and allergies, much remains unknown about how GPCR-induced signaling cascades are regulated in the immune system. Our section focuses on the role of regulator of G protein signaling (RGS) proteins in immune effector cells that mediate allergic responses (mainly mast cells and T lymphocytes) We use mouse models of allergic inflammation to assess the trafficking and activation of these cells and the effect of genetic manipulation of RGS expression in transgenic and knockout mice. Through genetic and biochemical studies, we recently discovered that one of these proteins, RGS13, suppressed anaphylactic responses in mice by inhibiting the assembly of a multiprotein signaling complex in mast cells induced by allergen exposure.
We are also interested in the function of RGS proteins in the modulation of bronchial smooth muscle tone in normal and disease states and are utilizing RNA interference technology to modify RGS expression in primary smooth muscle cells and in mice.
Major Areas of Research
- Regulation of the signaling pathways induced by G-protein-coupled receptors (GCPRs)
- Mast cell and lymphocyte trafficking in allergic inflammation
- GPCR-induced airway smooth muscle contractility in asthma
Research Group Members
Zhihui (Sherry) Xie, Ph.D; Jeffrey DiVietro, Ph.D., Genqing Liang, Ph.D., Yunbiao Lu, Ph.D.; Zhao Yang, Ph.D.
Selected Recent Publications
To view a complete listing, visit PubMed.
Xie Z, Geiger TR, Johnson EN, Nyborg JK, Druey KM. RGS13 acts as a nuclear repressor of CREB. Mol Cell. 2008. In press.
Bansal G, Xie Z, Rao S, Nocka KH, Druey KM. Suppression of IgE-mediated allergic responses by regulator of G protein signaling 13. Nat Immunol. 2008 Jan;9(1):73-80.
Castellone MD, Teramoto H, Williams BO, Druey KM, Gutkind JS. Prostaglandin E2 promotes colon cancer cell growth through a Gs-axin-beta-catenin signaling axis. Science. 2005 Dec 2;310(5753):1504-10.
Estes JD, Thacker TC, Hampton DL, Kell SA, Keele BF, Palenske EA, Druey KM, Burton GF. Follicular dendritic cell regulation of CXCR4-mediated germinal center CD4 T cell migration. J Immunol. 2004 Nov 15;173(10):6169-78.
Johnson EN, Seasholtz TM, Waheed AA, Kreutz B, Suzuki N, Kozasa T, Jones TL, Brown JH, Druey KM. RGS16 inhibits signaling through the G13-Rho axis. Nat Cell Biol. 2003 Dec;5(12):1095-103.
Lippert E, Yowe DL, Gonzalo JA, Justice JP, Webster JM, Fedyk ER, Hodge M, Miller C, Gutierrez-Ramos JC, Borrego F, Keane-Myers A, Druey KM. Role of RGS16 in inflammation-induced T lymphocyte migration and activation. J Immunol. 2003 Aug 1;171(3):1542-55.
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