ArticleProceedings of the National Academy of Sciences of the United States of America1991
A small region of the beta-adrenergic receptor is selectively involved in its rapid regulation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 172 citations in OpenAlex.
- Spinal motoneuron excitability is homeostatically regulated through β-adrenergic neuromodulation in wild-type and presymptomatic SOD1 mice.Progress in neurobiology · 2026Article
- Conformational biosensors delineate endosomal G protein regulation by GPCRs.Nature communications · 2026Article
- Intersection of GPCR trafficking and cAMP signaling at endomembranes.The Journal of cell biology · 2025Review
- Genetic variants of accessory proteins and G proteins in human genetic disease.Critical reviews in clinical laboratory sciences · 2025Review
- Discrete GPCR-triggered endocytic modes enable β-arrestins to flexibly regulate cell signaling.eLife · 2022Article
- Proteomic Approaches to Investigate Regulated Trafficking and Signaling of G Protein-Coupled Receptors.Molecular pharmacology · 2021Review
- Genetic evidence that β-arrestins are dispensable for the initiation of βScience signaling · 2017Article
- Optodynamic simulation of β-adrenergic receptor signalling.Nature communications · 2015Article
- G protein-coupled receptor (GPCR) signaling via heterotrimeric G proteins from endosomes.The Journal of biological chemistry · 2015Review
- Investigating signaling consequences of GPCR trafficking in the endocytic pathway.Methods in enzymology · 2014Article
- Reprogramming of G protein-coupled receptor recycling and signaling by a kinase switch.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Article
- G-protein coupled receptor resensitization-appreciating the balancing act of receptor function.Current molecular pharmacology · 2012Article
- A common intracellular allosteric binding site for antagonists of the CXCR2 receptor.British journal of pharmacology · 2010Article
- Cargo-mediated regulation of a rapid Rab4-dependent recycling pathway.Molecular biology of the cell · 2009Article
- Role of adiponectin in human skeletal muscle bioenergetics.Cell metabolism · 2006Article
- Multifaceted roles of beta-arrestins in the regulation of seven-membrane-spanning receptor trafficking and signalling.The Biochemical journal · 2003Review
- Distinct dynamin-dependent and -independent mechanisms target structurally homologous dopamine receptors to different endocytic membranes.The Journal of cell biology · 1999Article
- From the H(2) receptor gene to reclassification of the H(2) receptor antagonists.Inflammopharmacology · 1998Article
- Ligand-induced internalization of cholecystokinin receptors. Demonstration of the importance of the carboxyl terminus for ligand-induced internalization of the rat cholecystokinin type B receptor but not the type A receptor.The Journal of biological chemistry · 1997Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Plasma membrane receptors that couple to guanine nucleotide-binding regulatory proteins (G proteins) undergo a variety of rapid (minutes) and longer term (hours) regulatory processes induced by ligands. For the beta 2-adrenergic receptor (beta 2AR), the rapid processes include functional desensitization, mediated by phosphorylation of the receptor by the cAMP-dependent protein kinase and the beta-adrenergic receptor kinase, as well as a loss of hydrophilic ligand binding proposed to represent sequestration of receptors into a cellular compartment distinct from the plasma membrane. The slower processes include beta 2AR down-regulation (i.e., a decrease in the total cellular complement of receptors). It is not yet known whether beta 2AR phosphorylation and/or sequestration are prerequisites for down-regulation of the receptor. Like other G protein-coupled receptors, the beta 2AR molecule spans the plasma membrane seven times, and the cytoplasmic carboxyl-terminal domain has been proposed to contain molecular determinants for each of these regulatory processes. We replaced four serine and threonine residues located within a 10-amino acid segment of this domain of beta 2AR and thereby prevented agonist-promoted phosphorylation, sequestration, and rapid desensitization of the adenylyl cyclase response. In contrast, these mutations did not affect functional coupling to the stimulatory G protein Gs or long-term down-regulation. These findings thus define a small, hitherto unappreciated region of the receptor molecule that may selectively subserve its rapid regulation. In addition, with the demonstration that beta 2AR does not have to be phosphorylated or sequestered in order to enter the down-regulation pathway, the results suggest that the classical receptor endocytosis model may not be appropriate for beta 2AR regulation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.