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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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Genomic organization of adrenergic and serotonin receptors in the mouse: linkage mapping of sequence-related genes provides a method for examining mammalian chromosome evolution.

TL;DR: A region that may have been translocated during evolution is identified and it is suggested that the human genomic organization of adrenergic receptors more closely resembles that of a putative primordial ancestor.
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Mechanism of beta2AR regulation by an intracellular positive allosteric modulator.

TL;DR: The crystal structure of the prototypic β 2 -adrenergic receptor in complex with an orthosteric agonist and compound-6FA, a positive allosteric modulator of this receptor is reported, revealing a pocket created by intracellular loop 2 and transmembrane segments 3 and 4, stabilizing the loop in an α-helical conformation required to engage the G protein.
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Functional integrity of desensitized beta-adrenergic receptors.

TL;DR: Assessment of the functionality of the sequestered vesicular receptors by fusing them to Xenopus laevis erythrocytes demonstrates that beta-adrenergic receptors internalized during desensitization retain their functionality when recoupled to an adenylate cyclase system from a different source.
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Altered airway and cardiac responses in mice lacking G protein-coupled receptor kinase 3.

TL;DR: Data demonstrate that in the mouse, GRK3 may be involved in modulating the cholinergic response of airway smooth muscle and in regulating the chronotropic component of the baroreceptor reflex.
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The impact of aging on adrenergic receptor function: clinical and biochemical aspects.

TL;DR: In this paper, it was shown that with advancing age there is a decrease in cardiovascular responsiveness and, more specifically, there is an increase in catecholamine-stimulated chronotropic and inotropic responses.