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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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β-Arrestin-mediated PDE4 cAMP phosphodiesterase recruitment regulates β-adrenoceptor switching from Gs to Gi

George S. Baillie, +6 more
- 04 Feb 2003 - 
TL;DR: Receptor-stimulated β-arrestin-mediated recruitment of PDE4 plays a central role in the regulation of G protein switching by the β2AR in a physiological system, the cardiac myocyte.
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The Stability of the G Protein-coupled Receptor-β-Arrestin Interaction Determines the Mechanism and Functional Consequence of ERK Activation *

Akira Tohgo, +8 more
- 21 Feb 2003 - 
TL;DR: The C-terminal tail of a GPCR, by determining the stability of the receptor-β-arrestin complex, controls the extent of β-Arrestin-bound ERK activation, and influences both the subcellular localization of activated ERK and the physiologic consequences of ERKactivation.
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beta-Arrestin 1 and 2 differentially regulate heptahelical receptor signaling and trafficking.

Trudy A. Kohout, +4 more
- 13 Feb 2001 - 
TL;DR: Results suggest that sequestration of various heptahelical receptors is regulated differently by the two beta-arrestins, whereas both isoforms are capable of supporting receptor desensitization and down-regulation.
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A β-arrestin 2 Signaling Complex Mediates Lithium Action on Behavior

Jean-Martin Beaulieu, +10 more
- 11 Jan 2008 - 
TL;DR: Lithium, a pharmacological agent used for the management of psychiatric disorders such as bipolar disorder, schizophrenia, and depression, regulates Akt/glycogen synthase kinase 3 (GSK3) signaling and related behaviors in mice by disrupting a signaling complex composed of Akt, beta-arrestin 2, and protein phosphatase 2A.
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Functional antagonism of different G protein-coupled receptor kinases for β-arrestin-mediated angiotensin II receptor signaling

Jihee Kim, +6 more
- 01 Feb 2005 - 
TL;DR: Findings indicate distinct functional capabilities of beta-arrestins bound to receptors phosphorylated by different classes of GRKs, which are related to receptor recruitment, recruitment, and receptor endocytosis.