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Federico Mayor Jr.**, Elisa Lucas, María Jurado-Pueyo, Lucia Garcia-Guerrac, Iria Nieto-Vazquez, Rocio Vila-Bedmar, Sonia Fernández-Veledo & Cristina Murgaa Departamento de Biología Molecular and Centro de Biología Molecular Severo Ochoa (CSIC-UAM), 28049 Madrid (Spain)b Instituto de Investigación Sanitaria La Princesa, 28006 Madrid, Spainc Instituto de Investigaciones Biomédicas “Alberto Sols” (CSIC-UAM), Arturo Duperier, 4, 28029 Madridd Department of Biochemistry and Molecular Biology II, Faculty of Pharmacy, Complutense University, 28040 Madrid, Spaine Hospital Universitari de Tarragona Joan XXIII, IISPV, Universitat Rovira i Virgili, 43007 Tarragona, Spainf Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Matabólicas CIBERDEM, SpainThis work is dedicated to the memory of Professor Margarita Lorenzo, who passed away 7 April 2010, at the age of 51.Address for correspondence: Federico Mayor Jr, Universidad Autónoma Madrid, Centro de Biología Molecular, c/Nicolas Cabrera 1, Universidad Autonoma, Madrid, 28049 Spain. Tel:34-91-196-4626. Fax:34-91-196-4420. E-mail:fmayor@cbm.uam.esG protein-coupled receptor kinase 2 (GRK2) is emerging as a key, integrative node in many signalling pathways. Besides its canonical role in the modulation of the signalling mediated by many G protein-coupled receptors (GPCR), this protein can display a very complex network of functional interactions with a variety of signal transduction partners, in a stimulus, cell type, or context-specific way. We review herein recent data showing that GRK2 can regulate insulin-triggered transduction cascades at different levels and that this protein plays a relevant role in insulin resistance and obesity in vivo, what uncovers GRK2 as a potential therapeutic target in the treatment of these disorders.
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Mayor et al. (2011) studied this question.
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