ArticleNature chemical biology2025
Molecular basis of β-arrestin coupling to the metabotropic glutamate receptor mGlu3.
Article in Nature chemical biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Configurational diversity of metabotropic glutamate receptor complexes with beta-arrestins.Nature communications · 2026Article
- Structural basis of active state coupling of metabotropic glutamate receptor 8 to beta-arrestins.Nature communications · 2026Article
- Arrestins as programmable integrators of GPCR signaling: structural microstates, spatiotemporal logic, and therapeutic control.Cell discovery · 2026Review
- G protein selectivity in group I metabotropic glutamate receptors.Science advances · 2026Article
- Subtype-dependent arrestin engagement of the metabotropic glutamate receptors.Nature communications · 2026Article
- Cooperative Control of Arrestin Activation By Membrane Lipids And Phosphorylation Barcodes.bioRxiv : the preprint server for biology · 2026Article
- Phosphorylation site topology governs the functional dynamics of arrestin recruitment to GPCRs.Research square · 2026Article
- Cryo-EM Structures of Brain-Derived G Protein-Coupled Receptors: The First Direct Visualization from Mammalian Brain Tissue.bioRxiv : the preprint server for biology · 2026Article
- De novo design of GPCR exoframe modulators.Nature · 2026Article
- Banxia-Baizhu-Tianma Decoction Combined with Acupuncture for Cerebral Ischemic Stroke: A Narrative Review.International journal of general medicine · 2026Review
- Potential Roles of G Protein-Coupled Receptor 30 (GPR30) in Migraine Pathophysiology.Journal of pain research · 2026Review
- Stabilized DNature communications · 2025Article
- Unveiling the molecular mechanism of GProtein science : a publication of the Protein Society · 2025Article
- Mechanistic insights into the versatile stoichiometry and biased signaling of the apelin receptor-arrestin complex.Nature communications · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
β-Arrestins (βarrs) mediate the desensitization and internalization of activated G-protein-coupled receptors (GPCRs). The molecular mechanism by which dimeric family C GPCR members recruit arrestins remains elusive. Here we report two structures of metabotropic glutamate receptor subtype 3 (mGlu3) coupled to βarr1, with stoichiometries of 2:1 and 2:2. The L-glutamate-bound mGlu3 dimer adopts an inactive state, with both Venus flytrap domains closed, engaging βarr1 either asymmetrically or symmetrically. The transmembrane domain of the mGlu3 protomer interacts with βarr1 through a binding pocket formed by three intracellular loops and an ordered C-terminal region. Three phosphorylation sites (pS857, pS859 and pT860) on the C-terminal tail of mGlu3 engage the N domain of βarr1. βarr1 stabilizes mGlu3 in an inactive conformation, characterized by a TM3/TM4-TM3/TM4 dimeric interface, previously observed in the negative allosteric modulator-bound structure of mGlu3. Our findings provide important insights into βarr-mediated inactivation of family C GPCRs.
Indexed as
Identifiers
40050438What Socratic holds
Registered trials
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 Socratic graph.