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http://purl.uniprot.org/citations/34289359http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/34289359http://www.w3.org/2000/01/rdf-schema#comment"Many neurological disorders show an increased prevalence of GluA2-lacking, Ca2+-permeable AMPA receptors (CP-AMPARs), which dramatically alters synaptic function. However, the molecular mechanism underlying this distinct synaptic plasticity remains enigmatic. Here, we show that nerve injury potentiates postsynaptic, but not presynaptic, CP-AMPARs in the spinal dorsal horn via α2δ-1. Overexpressing α2δ-1, previously regarded as a Ca2+ channel subunit, augments CP-AMPAR levels at the cell surface and synapse. Mechanistically, α2δ-1 physically interacts with both GluA1 and GluA2 via its C terminus, inhibits the GluA1/GluA2 heteromeric assembly, and increases GluA2 retention in the endoplasmic reticulum. Consequently, α2δ-1 diminishes the availability and synaptic expression of GluA1/GluA2 heterotetramers in the spinal cord in neuropathic pain. Inhibiting α2δ-1 with gabapentin or disrupting the α2δ-1-AMPAR complex fully restores the intracellular assembly and synaptic dominance of heteromeric GluA1/GluA2 receptors. Thus, α2δ-1 is a pivotal AMPAR-interacting protein that controls the subunit composition and Ca2+ permeability of postsynaptic AMPARs."xsd:string
http://purl.uniprot.org/citations/34289359http://purl.org/dc/terms/identifier"doi:10.1016/j.celrep.2021.109396"xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/author"Chen H."xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/author"Li L."xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/author"Lee G."xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/author"Wang L."xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/author"Chen S.R."xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/author"Li D.P."xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/author"Pan H.L."xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/author"Zhou M.H."xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/author"Jayaraman V."xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/date"2021"xsd:gYear
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/name"Cell Rep"xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/pages"109396"xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/title"alpha2delta-1 switches the phenotype of synaptic AMPA receptors by physically disrupting heteromeric subunit assembly."xsd:string
http://purl.uniprot.org/citations/34289359http://purl.uniprot.org/core/volume"36"xsd:string
http://purl.uniprot.org/citations/34289359http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/34289359
http://purl.uniprot.org/citations/34289359http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/34289359
http://purl.uniprot.org/uniprot/#_A0A411ACY8-mappedCitation-34289359http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34289359
http://purl.uniprot.org/uniprot/#_E9Q1X8-mappedCitation-34289359http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34289359
http://purl.uniprot.org/uniprot/#_O08532-mappedCitation-34289359http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34289359
http://purl.uniprot.org/uniprot/#_Q14BH8-mappedCitation-34289359http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34289359
http://purl.uniprot.org/uniprot/#_Q3TQD0-mappedCitation-34289359http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34289359
http://purl.uniprot.org/uniprot/#_Q8C6Y3-mappedCitation-34289359http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34289359