Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

β-Arrestin2 Couples Metabotropic Glutamate Receptor 5 to Neuronal Protein Synthesis and Is a Potential Target to Treat Fragile X.

Cell reports - 21 Mar 2017

Stoppel Laura J, Auerbach Benjamin D, Senter Rebecca K, Preza Anthony R, Lefkowitz Robert J, Bear Mark F

Abstract excerpt

Synaptic protein synthesis is essential for modification of the brain by experience and is aberrant in several genetically defined disorders, notably fragile X (FX), a heritable cause of autism and intellectual disability. Neural activity directs local protein synthesis via activation of metabotropic glutamate receptor 5 (mGlu5), yet how mGlu5 couples to the intracellular signaling pathways that regulate mRNA...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to beta-Arrestin 2
Share to Dizocilpine Maleate

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Extracellular Signal-Regulated MAP Kinases

Share to Fragile X Mental Retardation Protein

Share to GTP-Binding Protein alpha Subunits, Gq-G11

Share to Locomotion

Share to Neuronal Plasticity

Share to Receptor, Metabotropic Glutamate 5

Source

Open in PubMed Open full text

Identifiers

PMID: 28329674
DOI: 10.1016/j.celrep.2017.02.075
PMCID: PMC5391046

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

β-Arrestin2 Couples Metabotropic Glutamate Receptor 5 to Neuronal Protein Synthesis and Is a Potential Target to Treat Fragile X.PMID 28329674Read ↗

Chronic pharmacological mGlu5 inhibition corrects fragile X in adult mice.Semantic proximity Read ↗

Genetic removal of p70 S6 kinase 1 corrects molecular, synaptic, and behavioral phenotypes in fragile X syndrome mice.Semantic proximity Read ↗

Investigating potential treatment strategies and underlying mechanisms in the Fragile X Syndrome mouse and rat modelsSemantic proximity Read ↗

Mutations causing syndromic autism define an axis of synaptic pathophysiology.Semantic proximity Read ↗

Metabotropic glutamate receptors and fragile x mental retardation protein: partners in translational regulation at the synapse.Semantic proximity Read ↗

mGluR5 Negative Modulators for Fragile X: Resistance and PersistenceSemantic proximity Read ↗

Learning and memory deficits consequent to reduction of the fragile X mental retardation protein result from metabotropic glutamate receptor-mediated inhibition of cAMP signaling in Drosophila.Semantic proximity Read ↗

Translational modulation by ISRIB alleviates synaptic and behavioral phenotypes in Fragile X syndromeSemantic proximity Read ↗

Genetic deletion of regulator of G-protein signaling 4 (RGS4) rescues a subset of fragile X related phenotypes in the FMR1 knockout mouse.Semantic proximity Read ↗

Targeting Translation Control with p70 S6 Kinase 1 Inhibitors to Reverse Phenotypes in Fragile X Syndrome Mice.Semantic proximity Read ↗

Selective Disruption of Metabotropic Glutamate Receptor 5-Homer Interactions Mimics Phenotypes of Fragile X Syndrome in Mice.Semantic proximity Read ↗

Altered synaptic plasticity in a mouse model of fragile X mental retardation.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.