R
Robert J. Lefkowitz
Researcher at Howard Hughes Medical Institute
Publications - 867
Citations - 153371
Robert J. Lefkowitz is an academic researcher from Howard Hughes Medical Institute. The author has contributed to research in topics: Receptor & G protein-coupled receptor. The author has an hindex of 214, co-authored 860 publications receiving 147995 citations. Previous affiliations of Robert J. Lefkowitz include University of Nice Sophia Antipolis & University of Stuttgart.
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Differential Kinetic and Spatial Patterns of β-Arrestin and G Protein-mediated ERK Activation by the Angiotensin II Receptor
TL;DR: In this paper, the authors distinguish the kinetic and spatial patterns that characterize ERK1/2 activated by either G protein (G(q)/G(11) or beta-arrestin2.
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Specific receptor sites for chemotactic peptides on human polymorphonuclear leukocytes
TL;DR: Data indicate that fMet-Leu-[3H]Phe can be used to identify binding sites for chemotactic peptides on human polymorphonuclear leukocytes and it is likely that these binding sites initiate the specific response of motile cells to N-formylmethionyl peptides.
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Cross-talk between cellular signalling pathways suggested by phorbol-ester-induced adenylate cyclase phosphorylation.
Takaaki Yoshimasa,Takaaki Yoshimasa,David R. Sibley,Michel Bouvier,Robert J. Lefkowitz,Marc G. Caron +5 more
TL;DR: The first direct demonstration of a covalent modification of the catalytic unit of adenylate cyclase is provided, providing a potential biochemical mechanism for a regulatory link between the two major transmembrane signalling systems.
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Expression of a β-adrenergic receptor kinase 1 inhibitor prevents the development of myocardial failure in gene-targeted mice
Howard A. Rockman,Kenneth R. Chien,Dong-Ju Choi,Guido Iaccarino,John J. Hunter,John Ross,Robert J. Lefkowitz,Walter J. Koch +7 more
TL;DR: The striking finding that overexpression of this inhibitor prevents the development of cardiomyopathy in this murine model of heart failure is reported, implicate abnormal betaAR-G protein coupling in the pathogenesis of the failing heart and point the way toward development of agents to inhibit betaARK1 as a novel mode of therapy.
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Targeting of Cyclic AMP Degradation to β2-Adrenergic Receptors by β-Arrestins
Stephen J. Perry,George S. Baillie,Trudy A. Kohout,Ian McPhee,Maria M. Magiera,Kok Long Ang,William E. Miller,Alison J. McLean,Marco Conti,Miles D. Houslay,Robert J. Lefkowitz +10 more
TL;DR: It is shown that β-arrestins coordinate both processes by recruiting PDEs to activated β2-adrenergic receptors in the plasma membrane of mammalian cells by simultaneously slowing the rate of cAMP production through receptor desensitization and increasing the rates of its degradation at the membrane.