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 Laboratory of Immunoregulation, NIAID. He joined the Laboratory of Allergic Diseases in 1997 to become acting head of the Molecular Signal Transduction Section (MSTS).

Description of Research Program

The primary focus of our laboratory is signaling mediated by G-protein-coupled receptors (GPCRs) and the role of specific GPCRs in the pathogenesis of asthma. Although antagonists or agonists of GPCRs have long been a mainstay of anti-asthma therapy, we understand very little about how these pathways are regulated in the immune system and the contribution of specific pathways to allergic inflammation. To address these issues, we are evaluating the role of certain RGS proteins in the function of leukocytes contributing to the inflammatory response (T cells and mast cells). We employ mouse models of allergic pulmonary inflammation to assess the trafficking and activation of these cells and the effect of genetic manipulation of RGS expression in transgenic and knockout mice.

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 signaling mediated by heterotrimeric G proteins
• Role of RGS proteins in leukocyte trafficking in allergic inflammation
• Role of G proteins and RGS proteins in bronchial reactivity in asthma

Research Group Members

Mourad Majidi, Ph.D.; Geetanjali Bansal, Ph.D.; Vonnie Gant.

Selected Recent Publications

To view a complete listing, visit PubMed.

Druey KM. Regulators of G protein signaling (RGS proteins): potential targets for the treatment of allergic inflammatory diseases such as asthma. Exp Opin on Ther Targ. 2003. 7: 475-84.

Lippert E, Yowe DL, Gonzalo J-A, Justice JP, Webster JM, Fedyk E, 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. 171: 1542-55.

Osterhout JL, Waheed AA, Hiol A, Ward RJ, Davey PC, Nini L, Wang J, Milligan G, Jones TLZ, Druey KM. Palmitoylation regulates RGS16 function II. Palmitoylation of a cysteine residue in the RGS box is critical for RGS16 GTPase accelerating activity and regulation of Gi-coupled signaling. J Biol Chem. 2003. 278: 19309-19316.

Derrien A, Zheng B, Osterhout JL, Ma YC, Milligan G, Farquhar MG, Druey KM. Src-mediated RGS16 tyrosine phosphorylation promotes RGS16 stability. J Biol Chem. 2003. 278: 16107-16116.

Johnson EN, Druey KM. Functional characterization of the G protein regulator RGS13. J Biol Chem. 2002. 277: 16768-16774.

Druey KM. Bridging with GAPs: receptor communication through RGS proteins. Science. 2001. STKE 2001:RE14.

Derrien A, Druey KM. RGS16 function is regulated by epidermal growth factor-mediated tyrosine phosphorylation. J Biol Chem. 276: 48532-48538.

Johnson EN, Seasholtz TM, Waheed A, Kreutz B, Suzuki N, Kozasa T, Jones TLZ, Brown JH, Druey KM. RGS16 inhibits signaling through the Gα13-Rho axis. Nature Cell Biol. In press 2003.

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