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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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Inhibition of the beta-adrenergic receptor kinase by polyanions.
TL;DR: The identification of compounds which specifically inhibit beta-adrenergic receptor kinase should prove useful in further defining the biological role of this enzyme.
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Targeting Gbeta gamma signaling in arterial vascular smooth muscle proliferation: a novel strategy to limit restenosis.
TL;DR: In vivo results demonstrated that the presence of the betaARKct in injured rat carotid arteries significantly reduced VSM intimal hyperplasia by 70%, and targeted Gbetagamma inhibition represents a novel approach for the treatment of pathological conditions such as restenosis.
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Beta-adrenergic receptors: recognition and regulation.
TL;DR: Of the various endogenous hormones and exogenous drugs, few have more widespread and potent effects than the catecholamines, and they are among the most useful and versatile agents at the physician's disposal.
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Effect of Cellular Expression of Pleckstrin Homology Domains on Gi-coupled Receptor Signaling
Louis M. Luttrell,Brian E. Hawes,Kazushige Touhara,Tim van Biesen,Walter J. Koch,Robert J. Lefkowitz +5 more
TL;DR: The data suggest that the PH domain peptides behave as specific antagonists of Gβγ-mediated signaling in intact cells and that interactions between PH domains and G βγ subunits or structurally related proteins may play a role in the activation of mitogenic signaling pathways by G protein-coupled receptors.
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In vitro desensitization of beta adrenergic receptors in human neutrophils. Attenuation by corticosteroids.
TL;DR: S steroids appeared to attenuate agonist-induced desensitization of thebeta adrenergic receptor-adenylate cyclase system by dampening the ability of agonists to uncouple receptors without modifying their ability to promote down-regulation of beta adrenergic receptors.