scispace - formally typeset
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.

Papers
More filters
Journal ArticleDOI

Overview of the Alliance for Cellular Signaling.

Alfred G. Gilman, +76 more
- 12 Dec 2002 - 
TL;DR: The Alliance for Cellular Signaling will study intensively in two cells — B lymphocytes (the cells of the immune system) and cardiac myocytes — to facilitate quantitative modelling.
Journal ArticleDOI

The active conformation of beta-arrestin1: direct evidence for the phosphate sensor in the N-domain and conformational differences in the active states of beta-arrestins1 and -2.

TL;DR: This study determines conformational changes in beta-arrestin1 using limited tryptic proteolysis and matrix-assisted laser desorption ionization time-of-flight mass spectrometry analysis in the presence of a phosphopeptide derived from the C terminus of the V(2) vasopressin receptor or the corresponding unphosphorylated peptide (V( 2)Rnp).
Journal ArticleDOI

Agonist-induced increase in apparent β-adrenergic receptor size

TL;DR: The low concentrations of agonist that are capable of altering apparent receptor size and the sensitivity of this effect to guanyl nucleotides suggest that these phenomena may be intimately involved in eliciting the physiological effects of β-adrenergic catecholamines at the molecular level.
Journal ArticleDOI

G protein beta gamma subunits stimulate phosphorylation of Shc adapter protein

TL;DR: Results suggest that G beta gamma-stimulated Shc phosphorylation represents an early step in the pathway leading to p21ras activation, similar to the mechanism utilized by growth factor tyrosine kinase receptors.
Journal ArticleDOI

Prolonged kappa opioid receptor phosphorylation mediated by G-protein receptor kinase underlies sustained analgesic tolerance.

TL;DR: The coincident reversal of analgesic tolerance and slow return to a basal phosphorylation state matched the regeneration rate of functional kappa receptors following irreversible antagonism and suggested that receptor replacement rather than dephosphorylation was required to restore sensitivity.