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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Journal ArticleDOI
Cloning of the gene and cDNA for mammalian β -adrenergic receptor and homology with rhodopsin
Richard A. F. Dixon,Brian K. Kobilka,David J. Strader,Jeffrey L. Benovic,Henrik G. Dohlman,Thomas Frielle,Mark A. Bolanowski,Carl D. Bennett,Elaine Rands,Ronald E. Diehl,Richard A. Mumford,Eve E. Slater,Irving S. Sigal,Marc G. Caron,Robert J. Lefkowitz,Catherine D. Strader +15 more
TL;DR: Cloning of the gene and cDNA for the mammalian β2AR indicates significant amino-acid homology with bovine rhodopin and suggests that, like rhodopsin7, βAR possesses multiple membrane-spanning regions.
Journal Article
International Union of Pharmacology nomenclature of adrenoceptors.
David B. Bylund,D C Eikenberg,J P Hieble,S.Z. Langer,Robert J. Lefkowitz,Kenneth P. Minneman,P B Molinoff,R R Ruffolo,U Trendelenburg +8 more
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Beta-arrestin: a protein that regulates beta-adrenergic receptor function
TL;DR: It is proposed that beta-arrestin in concert with beta ARK effects homologous desensitization of beta-adrenergic receptors.
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The role of β-arrestins in the termination and transduction of G-protein-coupled receptor signals
TL;DR: In this article, the Src family tyrosine kinases and components of the ERK1/2 and JNK3 MAP kinase cascades are recruited to GPCR-occupied GPCRs by recruiting these kinases to the receptor.
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G protein-coupled receptors. III. New roles for receptor kinases and beta-arrestins in receptor signaling and desensitization.
TL;DR: New information suggests that receptor signaling and desensitization are in reality two intimately linked aspects of receptor function and that mechanisms previously viewed as “desensitizing” with respect to one signaling pathway may be “activating”with respect to another.