Research Topics
Genomes and Genes
| Kirk M DrueySummaryAffiliation: National Institutes of Health Country: USA Publications
| Collaborators
|
Detail Information
Publications
Heterotrimeric G protein signaling: role in asthma and allergic inflammationEric N Johnson
Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
J Allergy Clin Immunol 109:592-602. 2002....- Regulators of G protein signalling: potential targets for treatment of allergic inflammatory diseases such as asthmaKirk M Druey
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 2441 Parklawn Drive, Rockville, MD 20852, USA
Expert Opin Ther Targets 7:475-84. 2003..This review discusses the emerging functions of RGS proteins in immune processes and inflammatory states such as asthma, and their potential value as therapeutic targets for the treatment of allergic disease... 
Regulation of G-protein-coupled signaling pathways in allergic inflammationKirk M Druey
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, 10 Center Drive Room 11N242, Bethesda, MD 20892, USA
Immunol Res 43:62-76. 2009..In this review, we focus on some of the new regulatory elements that control the duration and amplitude of GPCR signal transduction pathways in immune effector cells and end-organ structural cells affected by allergic inflammation...- Regulator of G-protein signaling-5 inhibits bronchial smooth muscle contraction in severe asthmaZhao Yang
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Insitute of Allergy and Infectious Diseases NIH, 10 Center Drive, Bethesda, MD 20982, USA
Am J Respir Cell Mol Biol 46:823-32. 2012..These results suggest that increased RGS5 expression contributes to decreased myocyte shortening in severe and fatal asthma... - Narrative review: the systemic capillary leak syndromeKirk M Druey
National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, and Mayo Clinic College of Medicine, Rochester, Minnesota 20892, USA
Ann Intern Med 153:90-8. 2010..Much remains to be learned about SCLS, and clinicians should consider the diagnosis in patients with unexplained edema, increased hematocrit, and hypotension... - Palmitoylation regulates regulators of G-protein signaling (RGS) 16 function. I. Mutation of amino-terminal cysteine residues on RGS16 prevents its targeting to lipid rafts and palmitoylation of an internal cysteine residueAbel Hiol
Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 278:19301-8. 2003..L., Waheed, A. A., Hiol, A., Ward, R. J., Davey, P. C., Nini, L., Wang, J., Milligan, G., Jones, T. L. Z., and Druey, K. M. (2003) J. Biol. Chem. 278, 19309-19316) was critical for RGS16 and RGS4 GAP activity... - RGS13 controls g protein-coupled receptor-evoked responses of human mast cellsGeetanjali Bansal
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 181:7882-90. 2008..RGS13 overexpression inhibited CXCL12-evoked Ca(2+) mobilization, Akt phosphorylation and chemotaxis. These results suggest that RGS13 restricts certain GPCR-mediated biological responses of human mast cells... - RGS13 acts as a nuclear repressor of CREBZhihui Xie
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Mol Cell 31:660-70. 2008..B lymphocytes from Rgs13(-/-) mice had more beta(2)-agonist-induced OCA-B expression. Thus, RGS13 inhibits CREB-dependent transcription of target genes through disruption of complexes formed at the promoter... - Beta-agonist-associated reduction in RGS5 expression promotes airway smooth muscle hyper-responsivenessZhao Yang
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 286:11444-55. 2011..Repetitive β(2)-agonist use may not only lead to reduced bronchoprotection but also to sensitization of excitation-contraction signaling pathways as a result of reduced RGS5 expression... - RGS16 inhibits signalling through the G alpha 13-Rho axisEric N Johnson
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases National Institute of Health, Rockville, MD 20852, USA
Nat Cell Biol 5:1095-103. 2003..These results elucidate a new mechanism whereby a classical RGS protein regulates G alpha 13-mediated signal transduction independently of the RGS box... - RGS16 inhibits breast cancer cell growth by mitigating phosphatidylinositol 3-kinase signalingGenqing Liang
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 284:21719-27. 2009..These results suggest that the loss of RGS16 in some breast tumors enhances PI3K signaling elicited by growth factors and thereby promotes proliferation and TKI evasion downstream of HER activation... - Palmitoylation regulates regulator of G-protein signaling (RGS) 16 function. II. Palmitoylation of a cysteine residue in the RGS box is critical for RGS16 GTPase accelerating activity and regulation of Gi-coupled signallingJames L Osterhout
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20892, USA
J Biol Chem 278:19309-16. 2003..These results suggest that palmitoylation of a Cys residue in the RGS box is critical for RGS16 and RGS4 GAP activity and their ability to regulate Gi-coupled signaling in mammalian cells... - Phosphorylation of RGS13 by the cyclic AMP-dependent protein kinase inhibits RGS13 degradationZhihui Xie
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, NIAID NIH, 10 Center Drive, Room 11N242, Bethesda, MD 20892, USA
J Mol Cell Biol 2:357-65. 2010..Stabilization of RGS13 through PKA-mediated phosphorylation could enhance RGS13 functions, providing negative feedback regulation that promotes cellular desensitization... - p53 negatively regulates RGS13 protein expression in immune cellsShoko Iwaki
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 286:22219-26. 2011..These studies indicate that p53 may modulate immune responses through suppression of RGS13 transcription in MCs and B cells... - RGS16 attenuates pulmonary Th2/Th17 inflammatory responsesSucharita P Shankar
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 188:6347-56. 2012..Thus, RGS16-mediated confinement of T cells to Schistosome granulomas mitigates widespread cytokine-mediated pulmonary inflammation... - Naive T cells sense the cysteine protease allergen papain through protease-activated receptor 2 and propel TH2 immunityGenqing Liang
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
J Allergy Clin Immunol 129:1377-1386.e13. 2012..Basophils have the capacity to present antigen to naive T cells and promote T(H)2 differentiation directly or indirectly through IL-4 production... - Mouse and human eosinophils degranulate in response to platelet-activating factor (PAF) and lysoPAF via a PAF-receptor-independent mechanism: evidence for a novel receptorKimberly D Dyer
Section of Eosinophil Biology, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1883, USA
J Immunol 184:6327-34. 2010.... - Enhanced effector function of CD8(+) T cells from healthy controls and HIV-infected patients occurs through thrombin activation of protease-activated receptor 1Amanda Hurley
CMRS Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 1360, USA
J Infect Dis 207:638-50. 2013..These findings suggest that thrombin mediates cross-talk between the coagulation system and the adaptive immune system at sites of vascular injury through increased T-cell motility and production of proinflammatory cytokines... - Vascular endothelial hyperpermeability induces the clinical symptoms of Clarkson disease (the systemic capillary leak syndrome)Zhihui Xie
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Blood 119:4321-32. 2012..Our results support a model of SCLS pathogenesis in which nonimmunoglobulin humoral factors such as VEGF and Ang2 contribute to transient endothelial contraction, suggesting a molecular mechanism for this highly lethal disorder... - Role of regulator of G protein signaling 16 in inflammation-induced T lymphocyte migration and activationEric Lippert
Molecular Signal Transduction Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
J Immunol 171:1542-55. 2003..These results suggest that RGS16 may regulate T lymphocyte activation in response to inflammatory stimuli and migration induced by CXCR4, CCR3, and CCR5, but not CCR2 or CCR7... - Suppression of immunoglobulin E-mediated allergic responses by regulator of G protein signaling 13Geetanjali Bansal
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Immunol 9:73-80. 2008..Thus, RGS13 inhibits the assembly of immune receptor-induced signalosomes in mast cells. Abnormal RGS13 expression or function may contribute to disorders of amplified mast cell activity, such as idiopathic anaphylaxis... - R4 RGS proteins: regulation of G-protein signaling and beyondGeetanjali Bansal
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, United States
Pharmacol Ther 116:473-95. 2007.... - Prostaglandin E2 promotes colon cancer cell growth through a Gs-axin-beta-catenin signaling axisMaria Domenica Castellone
Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4340, USA
Science 310:1504-10. 2005..These findings may provide a molecular framework for the future evaluation of chemopreventive strategies for colorectal cancer... - Src-mediated RGS16 tyrosine phosphorylation promotes RGS16 stabilityAlexandrine Derrien
Laboratory of Allergic Diseases, NIAID National Institutes of Health, 12441 Parklawn Drive, Rockville, MD 20852, USA
J Biol Chem 278:16107-16. 2003..These results suggest that Src mediates RGS16 tyrosine phosphorylation, which may promote RGS16 stability... - Functional characterization of the G protein regulator RGS13Eric N Johnson
Molecular Signal Transduction Section, Laboratory of Allergic Diseases, NIAID, National Institutes of Health, Rockville, Maryland 20852, USA
J Biol Chem 277:16768-74. 2002..Surprisingly, RGS13 inhibits cAMP generation elicited by stimulation of the beta(2)-adrenergic receptor. These data suggest that RGS13 may regulate Galpha(i)-, Galpha(q)-, and Galpha(s)-coupled signaling cascades... - Follicular dendritic cell regulation of CXCR4-mediated germinal center CD4 T cell migrationJacob D Estes
Department of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84602, USA
J Immunol 173:6169-78. 2004..Thus, FDCs appear to directly affect GC T cell migration within lymphoid follicles... - Concerted stimulation and deactivation of pertussis toxin-sensitive G proteins by chimeric G protein-coupled receptor-regulator of G protein signaling 4 fusion proteins: analysis of the contribution of palmitoylated cysteine residues to the GAP activity oDaljit S Bahia
Molecular Pharmacology Group, Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow, UK
J Neurochem 85:1289-98. 2003.... - RGS3 interacts with 14-3-3 via the N-terminal region distinct from the RGS (regulator of G-protein signalling) domainJiaxin Niu
Department of Pharmacology, University of Illinois at Chicago College of Medicine, Chicago, IL 60612, U S A
Biochem J 365:677-84. 2002..This study describes a new level in the regulation of G-protein signalling, in which the inhibitors of G-proteins, RGS proteins, can themselves be regulated by phosphorylation and binding 14-3-3...