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.
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Molecular mechanisms of receptor desensitization using the β -adrenergic receptor-coupled adenylate cyclase system as a model
TL;DR: New insights into the molecular mechanisms underlying desensitization have emerged from the study of the receptors coupled to the ubiquitous second messenger-generating system adenylate cyclase.
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Regulation of tyrosine kinase cascades by G-protein-coupled receptors.
TL;DR: Three types of scaffolds for GPCR-directed complex assembly have been identified: transactivated receptor tyrosine kinases, integrin-based focal adhesions, and GPCRs themselves, and nonreceptor tyrosines play an important role in each case.
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Role of beta gamma subunits of G proteins in targeting the beta-adrenergic receptor kinase to membrane-bound receptors.
Julie A. Pitcher,James Inglese,Joyce B. Higgins,Jeffery L. Arriza,Patrick J. Casey,Chong Kim,Jeffery L. Benovic,Madan M. Kwatra,Marc G. Caron,Robert J. Lefkowitz +9 more
TL;DR: The rate and extent of the agonist-dependent phosphorylation of beta 2-adrenergic receptors and rhodopsin by Beta ARK are markedly enhanced on addition of G protein beta gamma subunits, suggesting that the enzyme preferentially binds specific beta gamma complexes.
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β-Arrestin-dependent, G Protein-independent ERK1/2 Activation by the β2 Adrenergic Receptor
Sudha K. Shenoy,Matthew T. Drake,Christopher D. Nelson,Daniel A. Houtz,Kunhong Xiao,Srinivasan Madabushi,Eric Reiter,Eric Reiter,Richard T. Premont,Olivier Lichtarge,Robert J. Lefkowitz +10 more
TL;DR: It is demonstrated that the β2AR can signal to ERK via a GRK5/6-β-arrestin-dependent pathway, which is independent of G protein coupling, and GRK2, membrane translocation of which requires Gβγ release upon G protein activation, was ineffective unless it was constitutively targeted to the plasma membrane by a prenylation signal.