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
Agonist-dependent phosphorylation of the alpha 2-adrenergic receptor by the beta-adrenergic receptor kinase.
Jeffrey L. Benovic,John W. Regan,H. Matsui,Federico Mayor,Susanna Cotecchia,L. M.F. Leeb-Lundberg,Marc G. Caron,Robert J. Lefkowitz +7 more
TL;DR: The results suggest that receptors coupled to either stimulation or inhibition of adenylate cyclase may be regulated by an agonist-dependent phosphorylation mediated by the beta-adrenergic receptor kinase.
Journal ArticleDOI
Regulation of V2 vasopressin receptor degradation by agonist-promoted ubiquitination.
TL;DR: Data suggest that V2R levels are regulated through at least two processes, in the absence of agonist stimulation, a slow degradative pathway operates that is independent of receptor ubiquitination, however, receptor stimulation leads to rapid β-arrestin2-dependent ubiquitinations of the receptor and increased degradation.
Journal ArticleDOI
Spinophilin blocks arrestin actions in vitro and in vivo at G protein-coupled receptors.
Qin Wang,Jiali Zhao,Ashley E. Brady,Jian Feng,Patrick B. Allen,Robert J. Lefkowitz,Paul Greengard,Lee E. Limbird +7 more
TL;DR: Spinophilin knockout mice were more sensitive than wild-type mice to sedation elicited by stimulation of α2 adrenergic receptors, whereas arrestin 3 knockout micewere more resistant, indicating that the signal-promoting, rather than the signals-terminating, roles of arrestin are more important for certain response pathways.
Journal ArticleDOI
A mutation of the beta 2-adrenergic receptor impairs agonist activation of adenylyl cyclase without affecting high affinity agonist binding. Distinct molecular determinants of the receptor are involved in physical coupling to and functional activation of Gs.
TL;DR: It is suggested that the molecular determinants of the beta 2-adrenergic receptor involved in formation of the ternary complex are not identical to those that transmit the agonist-induced stimulatory signal to Gs.
Journal ArticleDOI
A beta-adrenergic receptor kinase-like enzyme is involved in olfactory signal termination.
TL;DR: Heparin, an inhibitor of beta ARK, as well as anti-beta ARK-2 antibodies, completely prevents the rapid decline of second-messenger signals (desensitization) that follows odorant stimulation and strongly inhibits odorant-induced phosphorylation of olfactory ciliary proteins.