Nature Methods
- 5, 673 - 678 (2008)
Published online: 30 July 2008; | doi:10.1038/nmeth.1232
Engineering GPCR signaling pathways with RASSLsBruce R Conklin1, 2, Edward C Hsiao1, 2, 3, Sylvie Claeysen4, Aline Dumuis4, Supriya Srinivasan5, John R Forsayeth6, Jean-Marc Guettier7, W C Chang1, 8, Ying Pei9, Ken D McCarthy9, Robert A Nissenson1, 3, Jürgen Wess7, Joël Bockaert4 & Bryan L Roth91
Gladstone Institute of Cardiovascular Disease, 1650 Owens Street, San Francisco, California 94158, USA. 2
Departments of Medicine and Cellular and Molecular Pharmacology, University of California, San Francisco, 505 Parnassus Avenue, Room M994, San Francisco, California 94122, USA. 3
Endocrine Research Unit, Veterans Affairs Medical Center, and Departments of Medicine and Physiology, University of California, San Francisco, 4150 Clement Street, San Francisco, California 94121, USA. 4
Centre National de la Recherche Scientifique, UMR 5203, Institut de Génomique Fonctionnelle, 141 rue de la Cardonille and Institut National de la Santé et de la Recherche Médicale, U661, and Université Montpellier, 34094 Montpellier, France. 5
Department of Physiology, 600 16th St. University of California, San Francisco, San Francisco, California 94143, USA. 6
Department of Neurosurgery, University of California, San Francisco, MCB 226, 1855 Folsom Street, San Francisco, California 94103, USA. 7
Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892, USA. 8
Graduate Program in Pharmaceutical Sciences and Pharmacogenomics, University of California, San Francisco, 1700 Fourth Street, Byers Hall, Suite BH-216, San Francisco, California 94143, USA. 9
Department of Pharmacology, University of North Carolina, Chapel Hill, 1106 Mary Ellen Jones Building, CB 7365, 98 Manning Drive, Chapel Hill, North Carolina 27599, USA.
Correspondence should be addressed to Bruce R Conklin bconklin@gladstone.ucsf.edu or Bryan L Roth bryan_roth@med.unc.edu We are creating families of designer G protein–coupled receptors (GPCRs) to allow for precise spatiotemporal control of GPCR signaling in vivo. These engineered GPCRs, called receptors activated solely by synthetic ligands (RASSLs), are unresponsive to endogenous ligands but can be activated by nanomolar concentrations of pharmacologically inert, drug-like small molecules. Currently, RASSLs exist for the three major GPCR signaling pathways (Gs, Gi and Gq). We review these advances here to facilitate the use of these powerful and diverse tools.
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