Affinage

Showing GRIA2 — GLUR2 is a alias.

GRIA2

Glutamate receptor 2 · UniProt P42262

Length
883 aa
Mass
98.8 kDa
Annotated
2026-06-10
100 papers in source corpus 44 papers cited in narrative 44 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GRIA2 encodes GluA2, the AMPA-type glutamate receptor subunit that governs the Ca2+ permeability of fast excitatory synaptic transmission in the brain (PMID:8011338, PMID:7502080). The defining feature of GluA2 is an arginine introduced at the Q/R site of the channel pore by ADAR-catalyzed adenosine-to-inosine RNA editing, which depends on an imperfect exon-intron base-paired duplex in the pre-mRNA and renders heteromeric AMPARs Ca2+-impermeable (PMID:8269514, PMID:7502080); loss of this editing increases Ca2+ permeability and macroscopic conductance, producing seizures and lethality in mice (PMID:7502080, PMID:10195181), while restoring an edited (arginine) codon genomically is well tolerated, showing that Ca2+ permeability is set by the relative abundance of edited GluA2 (PMID:9811877). Rather than a binary impermeable channel, GluA2-containing AMPARs span a continuum of Ca2+ permeabilities tuned by subunit composition and auxiliary subunits (TARPs, cornichons) acting on the selectivity filter (PMID:40108453). GluA2 assembles as a tetrameric dimer-of-dimers ligand-gated cation channel (PMID:11705385) whose agonist-induced clamshell closure, gating, and desensitization, and their modulation by TARP γ2, are defined by crystal and cryo-EM structures (PMID:20713069, PMID:25109876, PMID:27368053). Surface delivery, retention, and degradation of GluA2 are controlled through its C-terminal domain by an NSF/PICK1/GRIP1 trafficking axis — NSF promotes membrane insertion (a step disrupted by Plk2 and requiring Q/R editing) (PMID:20534470, PMID:20802490), PICK1 mediates endosomal retention and an ER-exit step downstream of RAB39B and CaMKII/Ca2+ (PMID:22915106, PMID:24831007, PMID:25784538), and GRIP1 retains and recycles receptors via phospho-Y876 (PMID:21383172, PMID:32071234) — with additional control by β3 integrin binding, ubiquitination at Lys-870/882 directing lysosomal degradation, O-GlcNAcylation, and N-glycosylation at N370 and N413 (PMID:22232691, PMID:25660027, PMID:24381264, PMID:26271046). The GluA2 CTD is necessary and sufficient for NMDAR-dependent LTD and, through a membrane-proximal residue and phospho-Y876/GRIP1, for homeostatic synaptic upscaling (PMID:29230056, PMID:29180434, PMID:32071234), while the extracellular domain mediates a non-ionotropic role in mGluR-LTD via N-cadherin–Rac1–cofilin actin reorganization (PMID:21248105). De novo heterozygous GRIA2 mutations cause neurodevelopmental disorders, acting predominantly through loss-of-function reductions in receptor current but in some cases through gain-of-function gating changes (PMID:31300657, PMID:36161652).

Mechanistic history

Synthesis pass · year-by-year structured walk · 24 steps
  1. 1993 High

    Established how the Q/R editing site is recognized, answering how a single adenosine in GluA2 pre-mRNA is selected for site-specific modification.

    Evidence Mutagenesis of intronic and exonic complementary sequences with complementarity-restoring rescue in transfected PC12 cells

    PMID:8269514

    Open questions at the time
    • Did not identify the editing enzyme
    • Quantitative editing efficiency in vivo not addressed
  2. 1994 High

    Linked GluA2 (GluR-B) expression level to the Ca2+ permeability of native AMPARs, defining its physiological function in distinct neuron types.

    Evidence Patch-clamp plus single-cell mRNA analysis in neocortical brain slices

    PMID:8011338

    Open questions at the time
    • Did not separate editing from expression level
    • Subunit stoichiometry of native receptors not resolved
  3. 1995 High

    Proved in vivo that the edited arginine is essential for Ca2+ impermeability and survival, establishing editing as a non-redundant physiological requirement.

    Evidence Editing-incompetent GluR-B knock-in mice with electrophysiology and phenotyping

    PMID:7502080

    Open questions at the time
    • Cellular cause of seizures vs Ca2+ influx not dissected here
    • Developmental timing of requirement unclear
  4. 1995 High

    Identified the editing reaction biochemically as site-selective A-to-I deamination by a dsRNA adenosine deaminase, moving from genetics to enzyme mechanism.

    Evidence In vitro editing assay with HeLa nuclear extract and TLC nucleotide analysis

    PMID:7721757

    Open questions at the time
    • Specific ADAR isoform not pinpointed
    • Required cofactors not defined
  5. 1996 High

    Reconstituted editing with recombinant enzyme, showing duplex structure and a cofactor balance govern editing accuracy.

    Evidence In vitro editing with recombinant DRADA and purified GluR-B RNA

    PMID:8598204

    Open questions at the time
    • Cofactor identity not determined
    • ADAR1 vs ADAR2 contributions in neurons unresolved
  6. 1996 Medium

    Demonstrated that the isolated ligand-binding domain folds autonomously and binds agonist with native pharmacology independent of glycosylation, enabling structural study.

    Evidence Bacterial S1-S2 expression and [3H]AMPA radioligand binding

    PMID:8663017

    Open questions at the time
    • No structural model at this stage
    • Channel-coupled behavior not addressed
  7. 1998 High

    Showed unedited GluA2 is dispensable when an edited codon is supplied genomically, establishing that Ca2+ permeability is set by edited GluA2 abundance relative to other subunits.

    Evidence Exonic arginine knock-in mice with electrophysiology and phenotyping

    PMID:9811877

    Open questions at the time
    • Roles of editing kinetics in development not tested
    • Other editing sites not addressed
  8. 1999 High

    Dissected the disease mechanism of editing deficiency, attributing seizures to increased macroscopic conductance rather than Ca2+ influx per se.

    Evidence Allelic series of gene-targeted mice with patch-clamp and in vivo phenotyping

    PMID:10195181

    Open questions at the time
    • Circuit-level basis of epilepsy not resolved
    • Dendritic architecture defect mechanism unclear
  9. 2002 Medium

    Defined ADAR2 enzymology on GluA2 RNA — base-flipping, 5' duplex dependence, positioning over affinity, and homodimer requirement — explaining site selectivity.

    Evidence In vitro footprinting, kinetics, 2-aminopurine fluorescence, and RNA-dependent cross-linking (idx 8–11)

    PMID:10836790 PMID:11015203 PMID:12163487

    Open questions at the time
    • In vivo relevance of dimerization not tested
    • Regulation of editing levels in neurons not addressed
  10. 2001 Medium

    Established the quaternary architecture of GluA2 as a 2-fold symmetric dimer-of-dimers tetramer, the structural framework for later mechanistic studies.

    Evidence EM and biochemical characterization of purified GluR-B homomers

    PMID:11705385

    Open questions at the time
    • Low resolution; no domain-level detail
    • Heteromeric assembly not addressed
  11. 2007 Medium

    Showed RNA Pol II CTD coordinates editing-before-splicing, explaining how intronic ADAR2 recognition sequences are retained long enough for editing.

    Evidence Cell-based splicing/editing assays with CTD truncation minigenes

    PMID:17525170

    Open questions at the time
    • Direct molecular link between CTD and ADAR2 not defined
    • In vivo coupling not tested
  12. 2003 Medium

    Identified a GluA2(long)-specific, GluA1-independent route for activity- and LTP-driven synaptic AMPAR delivery, broadening models of plasticity.

    Evidence Viral overexpression, dominant-negatives, and slice electrophysiology with activity manipulation

    PMID:14687553

    Open questions at the time
    • Molecular determinants in the long tail not mapped
    • Adult vs juvenile differences unclear
  13. 2010 High

    Resolved the structural basis of agonist activation, desensitization, and allosteric modulation, defining the LBD as the conformational switch.

    Evidence X-ray crystallography of GluA2 S1S2 LBD with diverse ligands

    PMID:20713069

    Open questions at the time
    • Isolated LBD lacks intact-receptor context
    • Gating coupling to pore inferred indirectly
  14. 2010 High

    Defined the dual requirements — NSF binding and Q/R editing — for GluA2 plasma membrane insertion, and showed Plk2 gates this via NSF engagement.

    Evidence pHluorin-TIRF imaging of fusion events with domain mutants; Plk2-NSF Co-IP and electrophysiology (idx 15–16)

    PMID:20534470 PMID:20802490

    Open questions at the time
    • How editing influences insertion mechanistically unclear
    • Plk2 substrate other than NSF not excluded
  15. 2011 High

    Revealed a non-ionotropic GluA2 function in mGluR-LTD via extracellular N-cadherin–Rac1–cofilin signaling, separating channel-independent from channel-dependent roles.

    Evidence GluA2 KO, domain mutants, N-cadherin/Rac1/cofilin manipulations with slice LTD recordings

    PMID:21248105

    Open questions at the time
    • Structural basis of GluA2–N-cadherin contact not defined
    • Generality across synapse types untested
  16. 2012 High

    Established β3 integrin, S-SCAM/MAGI-2, and PICK1 as distinct controllers of synaptic GluA2 levels and homeostatic strength, expanding the trafficking interactome.

    Evidence Co-IP from brain, heterologous co-expression, RNAi, and electrophysiology (idx 20–22)

    PMID:22232691 PMID:22593065 PMID:22915106

    Open questions at the time
    • Hierarchy among these regulators unclear
    • Binding sites on GluA2 not all mapped
  17. 2014 High

    Captured intact-receptor conformations across resting, pre-open, and desensitized states and the TARP γ2-bound architecture, linking LBD motions to channel gating.

    Evidence Cryo-EM and DEER of full GluA2 in multiple functional states and GluA2–γ2 complex (idx 23, 33)

    PMID:25109876 PMID:27368053

    Open questions at the time
    • Heteromeric receptor structures not resolved here
    • Editing-site effect on pore not visualized
  18. 2014 Medium

    Defined multiple post-translational and post-transcriptional controls of GluA2 trafficking and supply (O-GlcNAcylation, Ca2+/PICK1 ER-exit, Sema3A/PlexA dendritic targeting, FXR1P translational repression).

    Evidence Biochemical detection, domain mutants, Co-IP, conditional KO, and electrophysiology across systems (idx 24–27)

    PMID:24381264 PMID:24599038 PMID:24831007 PMID:25456134

    Open questions at the time
    • O-GlcNAc sites on GluA2 not mapped
    • Enzymes responsible not all identified
  19. 2015 High

    Mapped ubiquitination sites (Lys-870/882) controlling lysosomal degradation, N-glycosylation sites (N370 ER exit, N413 HNK-1/N-cadherin), and the RAB39B–PICK1 ER-to-Golgi route, refining the GluA2 trafficking code.

    Evidence Site-directed mutagenesis, surface/endosome assays, Co-IP, RAB39B knockdown electrophysiology (idx 28–32)

    PMID:25660027 PMID:25784538 PMID:26271046

    Open questions at the time
    • E3 ligase for GluA2 not identified
    • GSK-3β/PICK1 phospho-control in vivo relevance partial
  20. 2017 High

    Demonstrated by reciprocal CTD-exchange knock-ins that the GluA2 CTD is necessary and sufficient for NMDAR-dependent LTD, and that a membrane-proximal tail region drives homeostatic upscaling.

    Evidence CTD-swap knock-in mice and viral domain-mutant rescue with LTP/LTD electrophysiology (idx 34–35)

    PMID:29180434 PMID:29230056

    Open questions at the time
    • Effector proteins reading the CTD during LTD not fully defined
    • Single critical residue identity narrow
  21. 2020 High

    Identified phospho-Y876 as the molecular switch coupling GluA2 to GRIP1 specifically during homeostatic scaling but not Hebbian plasticity, separating the two trafficking modes.

    Evidence Y876F phospho-deficient knock-in mice, scaling assays, and GluA2–GRIP1 Co-IP

    PMID:32071234

    Open questions at the time
    • Kinase/phosphatase acting on Y876 not defined
    • Other phospho-Y876 effectors not excluded
  22. 2018 High

    Showed both autoantibody-driven and RAB39B-dependent loss of synaptic GluA2 shift receptors toward Ca2+-permeable forms and impair plasticity and spine maturation, linking GluA2 trafficking to disease.

    Evidence Passive antibody transfer in mice and Rab39b KO with spine analysis, electrophysiology, and CP-AMPAR pharmacology (idx 36, 41)

    PMID:30146304 PMID:34035473

    Open questions at the time
    • Compensatory CP-AMPAR identity not fully defined
    • Reversibility/therapeutic windows untested
  23. 2019 High

    Established that de novo GRIA2 mutations cause neurodevelopmental disorders predominantly via loss-of-function reduced current, with gain-of-function gating mutations as a distinct, perampanel-sensitive subclass.

    Evidence Electrophysiology of 28 patient mutations and detailed characterization of A643V with pharmacology (idx 38, 42)

    PMID:31300657 PMID:36161652

    Open questions at the time
    • Genotype-phenotype correlation incomplete
    • In vivo modeling of individual variants limited
  24. 2025 High

    Reframed GluA2-containing AMPARs as a continuum of Ca2+ permeabilities tuned by composition and auxiliary subunits, revising the binary Ca2+-impermeable model.

    Evidence Patch-clamp across subunit and auxiliary-subunit combinations with identification of an extracellular Ca2+ docking site

    PMID:40108453

    Open questions at the time
    • Structural basis of the docking site not resolved here
    • Physiological consequences of the continuum in vivo untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How GluA2 trafficking regulators, editing status, and auxiliary-subunit composition are integrated in real time at individual synapses to set Ca2+ permeability and plasticity outcomes remains unresolved.
  • No unified model coupling editing, trafficking, and auxiliary-subunit control
  • E3 ligase and Y876 kinase identities unknown
  • Heteromeric receptor structures with editing site visualized lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 4 GO:0005215 transporter activity 3 GO:0005198 structural molecule activity 2
Localization
GO:0005886 plasma membrane 4 GO:0005783 endoplasmic reticulum 3 GO:0005768 endosome 2 GO:0005794 Golgi apparatus 1
Pathway
R-HSA-112316 Neuronal System 4 R-HSA-9609507 Protein localization 4 R-HSA-1643685 Disease 3 R-HSA-8953854 Metabolism of RNA 3
Partners
CDH2FXR1GRIP1ITGB3NSFPICK1PLXNARAB39B
Complex memberships
AMPA receptor (tetramer, dimer-of-dimers)GluA2-TARP γ2 (stargazin) complex

Evidence

Reading pass · 44 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 RNA editing at the Q/R site of GluR-B pre-mRNA requires a base-paired intron-exon structure: an imperfect inverted repeat in the proximal intron downstream of the unedited codon, containing a 10 nt sequence exactly complementary to the exon centered on the unedited codon, is essential for site-selective adenosine-to-inosine editing. Single nucleotide substitutions in either the intronic or exonic complementary sequences abolished editing, which was rescued by restoring complementarity. Transfection of GluR-B gene constructs into PC12 cells with targeted single-nucleotide substitutions and complementarity-restoring double mutations Cell High 8269514
1994 Differences in Ca2+ permeability of native AMPA-type glutamate receptor channels in neocortical neurons are caused by differential GluR-B subunit expression: pyramidal neurons express high GluR-B mRNA (Ca2+-impermeable receptors) while non-pyramidal neurons express low GluR-B mRNA (Ca2+-permeable receptors), as established by single-cell patch-clamp and single-cell mRNA analysis in brain slices. Patch-clamp recordings in brain slices combined with single-cell mRNA analysis (GluR-B/non-B ratio quantification) Neuron High 8011338
1995 The arginine at the Q/R site of GluR-B (introduced by RNA editing) is essential for rendering AMPA receptors Ca2+-impermeable in principal neurons in vivo. Mice engineered with an editing-incompetent GluR-B allele express unedited GluR-B, show increased AMPA receptor Ca2+ permeability in neurons, develop early-onset seizures, and die by 3 weeks. Gene targeting in mice (editing-incompetent GluR-B allele), electrophysiology, in vivo phenotypic analysis Science High 7502080
1995 GluR-B pre-mRNA Q/R and R/G sites are edited in vitro by nuclear extract via site-selective adenosine-to-inosine conversion, as confirmed by thin-layer chromatography of edited RNA sequences, implicating a double-stranded RNA adenosine deaminase (DRADA/ADAR). In vitro editing assay with HeLa nuclear extract; nucleotide analysis by thin-layer chromatography The Journal of biological chemistry High 7721757
1996 Recombinant DRADA (ADAR1/dsRNA adenosine deaminase) edits GLuR-B RNA at the Q/R site in vitro, but requires both a dsRNA structure (exon-intron duplex) and a cofactor protein present even in non-neuronal cells; the accuracy and efficiency of editing depend on the quantitative balance between DRADA, cofactor, and substrate RNA. In vitro editing assay using recombinantly expressed DRADA protein with purified GLuR-B RNA substrate The EMBO journal High 8598204
1996 The ligand-binding domain of GluR-B (S1-S2 fusion) expressed in E. coli binds [3H]AMPA with high affinity (Kd ~12 nM) and with pharmacology typical of native AMPA receptors; N-linked glycosylation is not required for formation or maintenance of the ligand-binding site. Bacterial expression of S1-S2 fusion protein; radioligand binding assay with [3H]AMPA The Journal of biological chemistry Medium 8663017
1998 The small amount of Q/R site-unedited GluR-B present in postnatal brain is not required for normal brain development or function; mice engineered with an exonic arginine codon at the Q/R site (bypassing RNA editing) show no obvious deficits, demonstrating that AMPA receptor Ca2+ permeability can be solely regulated by the levels of Q/R site-edited GluR-B relative to other AMPAR subunits. Gene targeting in mice (exonic arginine knock-in); electrophysiology; in vivo phenotypic analysis PNAS High 9811877
1999 Graded deficiency in GluR-B Q/R site editing in mice increases AMPA receptor Ca2+ permeability in pyramidal neurons and, at sufficient levels, induces NMDA receptor-independent LTP, epilepsy, and deficits in dendritic architecture. The seizure phenotype correlates with increased macroscopic AMPA receptor conductance rather than Ca2+ influx per se. Multiple gene-targeted mouse lines with varying GluR-B expression and editing levels; patch-clamp electrophysiology; in vivo phenotypic analysis Nature neuroscience High 10195181
2000 ADAR2 binds to the GluR-B R/G editing site RNA at a discrete region surrounding the editing site (as shown by footprinting), and binding affinity to wild-type versus editing-reduced mutant RNA is nearly identical, indicating that ADAR2 specificity is not determined by differential binding affinity but by positioning at the editing site. In vitro binding assays (gel shift, footprinting) with rat ADAR2 and synthetic GluR-B R/G site RNA substrates RNA Medium 10836790
2000 ADAR2-catalyzed editing of the GluR-B R/G site requires 5' duplex structure for efficient deamination; five base pairs of duplex 5' to the editing site increase single-turnover rate constant 17–39-fold. ADAR2 flips the reactive adenosine out of the helix prior to deamination, as evidenced by fluorescence enhancement of a 2-aminopurine-substituted substrate. In vitro deamination kinetics with synthetic substrates; fluorescence spectroscopy with 2-aminopurine analog Biochemistry High 11015203
2001 Purified GluRB homomeric channels are tetramers with molecular dimensions of approximately 11×14×17 nm and an overall 2-fold symmetric (dimer-of-dimers) assembly, as determined by electron microscopy of milligram-scale purified receptor. Density-gradient centrifugation; electron microscopy; ligand binding assays on purified GluRB homomers Biochemistry Medium 11705385
2002 ADAR2 functions as a homodimer on GluR-B R/G site RNA; a ternary ADAR2:RNA complex (two ADAR2 monomers) is required for efficient editing, and complex formation is rate-determining. ADAR monomers cross-link to each other in an RNA-dependent manner. Gel shift assay; RNA-dependent cross-linking; detailed kinetic analysis of editing reaction The Journal of biological chemistry Medium 12163487
2003 The GluR-B(long) splice variant of GluR-B mediates a GluR-A-independent form of glutamatergic synaptic plasticity in the juvenile hippocampus: spontaneous activity drives GluR-B(long) delivery maintaining ~1/3 of steady-state AMPA responses, while LTP induction drives GluR-B(long) delivery accounting for ~50% of potentiation at CA3-CA1 synapses. Viral overexpression, dominant-negative approaches, and electrophysiology in hippocampal slices; activity manipulation experiments Neuron Medium 14687553
2007 The C-terminal domain (CTD) of RNA Pol II coordinates editing and splicing of GluR-B pre-mRNA: the CTD is required for efficient ADAR2 editing at the R/G site by preventing premature splicing that would remove intronic ADAR2 recognition sequences, and it inhibits excision of intron 11 (which contains the Q/R editing complementary sequences), thereby enforcing the order editing-before-splicing. Cell-based splicing and editing assays with CTD truncation constructs; minigene transfection RNA Medium 17525170
2010 Crystal structures of the GluA2 ligand-binding domain in complex with agonists, antagonists, and positive allosteric modulators revealed the structural basis for receptor activation and desensitization: agonist binding induces clamshell closure of the S1-S2 domain, and positive allosteric modulators bind at the LBD dimer interface to stabilize the agonist-bound conformation and slow desensitization. X-ray crystallography of recombinant GluA2 S1S2 LBD; >80 structures reviewed including mutant and ligand-bound forms Neuropharmacology High 20713069
2010 GluA2 plasma membrane insertion requires: (1) the NSF-binding site within its intracellular C-terminal domain, and (2) Q/R site RNA editing in the ion channel region. Plasma membrane insertion of heteromeric GluA2/3 receptors follows the same rules as homomeric GluA2 receptors. pHluorin-tagged GluA2 with TIRF microscopy to visualize individual vesicle fusion events; domain mutants (NSF binding site deletion, Q/R site changes) PNAS High 20534470
2010 Polo-like kinase 2 (Plk2) directly interacts with NSF and disrupts the NSF-GluA2 interaction, promoting loss of surface GluA2 in hippocampal neurons, increased GluA2 association with PICK1 and GRIP1, and decreased synaptic AMPAR current. This mechanism requires Plk2-NSF engagement (via a novel Plk2 motif independent of the polo-box domain) but not Plk2 kinase activity. Co-immunoprecipitation; dominant-negative and kinase-dead constructs; electrophysiology in rat hippocampal neurons; surface biotinylation Nature neuroscience High 20802490
2011 GluA2 undergoes activity-dependent ubiquitination: increasing synaptic activity (bicuculline) or AMPA receptor agonists rapidly induces GluA2 ubiquitination, which requires clathrin- and dynamin-dependent endocytosis of AMPARs (ubiquitination occurs on plasma membrane AMPARs post-endocytosis). Immunoprecipitation of ubiquitinated proteins; pharmacological blockade of endocytosis; biochemical fractionation in cultured neurons The Journal of neuroscience Medium 21414928
2011 GluA2 regulates mGluR-dependent LTD through its extracellular domain interaction with N-cadherin, which activates Rac1 and cofilin-mediated actin reorganization. This non-ionotropic function of GluA2 is independent of its channel properties and required for mGluR-LTD in the hippocampus. GluA2 knockout neurons, domain-specific mutants, N-cadherin knockdown, Rac1/cofilin pathway manipulations; LTD recordings in hippocampal slices The Journal of neuroscience High 21248105
2011 GRIP1 variants found in autism patients alter GRIP1-GluA2/3 interaction via PDZ domains 4-6 and cause faster recycling and increased surface distribution of GluA2 in neurons (gain-of-function), whereas GRIP1/2 deficiency produces opposite effects on GluA2 surface levels. Biochemical interaction assays; surface GluA2 imaging in neurons; GRIP1/2 knockout mice PNAS Medium 21383172
2012 β3 integrin directly binds to the cytoplasmic domain of GluA2 (but only weakly to GluA1, and GluA1-β3 association requires GluA2 coexpression), forming a complex in mouse brain; this direct interaction underlies β3 integrin-dependent homeostatic control of synaptic GluA2 levels and synaptic strength. Co-immunoprecipitation from mouse brain; heterologous co-expression; electrophysiology in hippocampal pyramidal neurons; surface GluA2 measurement PNAS High 22232691
2012 S-SCAM/MAGI-2 maintains synaptic GluA2-containing AMPA receptors: increasing S-SCAM increases surface AMPAR levels and synaptic transmission in a GluA2-dependent (not GluA1-dependent), NSF-interaction-sensitive, and activity-independent manner; S-SCAM knockdown causes loss of synaptic AMPARs and spine density reduction. Overexpression and RNAi knockdown in rat hippocampal neurons; electrophysiology; surface AMPAR imaging The Journal of neuroscience Medium 22593065
2012 PICK1 binding to GluA2 on endosomal compartments restricts GluA2 from trafficking to the synaptic plasma membrane immediately after glycine stimulation (chemical LTP), enabling a transient switch to GluA2-lacking Ca2+-permeable AMPARs at synapses. Activation of CP-AMPARs then triggers release of GluA2 from PICK1, allowing GluA2-containing AMPARs to traffic back to the synaptic surface 5-20 min post-stimulus. Endogenous protein immunostaining, co-IP for PICK1-GluA2 binding; live-cell imaging; pharmacological blockade of CP-AMPARs in rat hippocampal neurons The Journal of neuroscience Medium 22915106
2014 Cryo-EM and DEER (double electron-electron resonance) structures of intact GluA2 AMPA receptor in apo/resting, activated/pre-open (partial agonist + positive allosteric modulator), and desensitized states revealed how agonist binding modulates LBD layer conformation and how desensitization involves large conformational rearrangements of both amino-terminal and ligand-binding domains. Cryo-electron microscopy; DEER EPR spectroscopy with cysteine mutants; structure determination in three distinct functional states Cell High 25109876
2014 O-GlcNAcylation of GluA2 is associated with a novel form of LTD at hippocampal synapses: acutely increasing O-GlcNAcylation induces NMDA receptor- and PKC-independent LTD that requires GluA2 subunits, and the GluA2 subunit is directly O-GlcNAcylated. Pharmacological O-GlcNAc elevation in hippocampal slices; LTD electrophysiology; GluA2 knockout rescue; direct O-GlcNAc immunoprecipitation of GluA2 The Journal of neuroscience Medium 24381264
2014 GluA2 trafficking from the endoplasmic reticulum to the plasma membrane requires Ca2+ release from internal stores (via IP3 and ryanodine receptors), CaMKII activity, and GluA2 interaction with PICK1 (via the PICK1 BAR domain). Ca2+ release promotes formation of a CaMKII-PICK1 complex that interacts with the GluA2 C-terminal domain to stimulate ER exit. Pharmacological inhibitors of IP3R and RyR; CaMKII inhibition; PICK1 domain mutants; surface trafficking assays in cultured hippocampal neurons The Journal of biological chemistry Medium 24831007
2014 Semaphorin 3A (Sema3A) retrograde signaling at the axonal growth cone drives GluA2 to distal dendrites via GRIP1-dependent localization; PlexinA (PlexA) interacts directly with GluA2 at its IPT domain in somatodendritic regions, and overexpression of PlexA-IPT suppresses GluA2 dendritic localization and induces abnormal proximal bifurcation of apical dendrites in CA1 neurons. Co-immunoprecipitation (PlexA-GluA2 interaction); knockdown of cytoplasmic dynein; overexpression of PlexA-IPT domain; immunostaining in hippocampal neurons Nature communications Medium 24599038
2014 FXR1P binds specifically to the 5' UTR of GluA2 mRNA to repress its translation; removal of FXR1P from mouse forebrain selectively enhances de novo GluA2 synthesis and increases GluA2 incorporation at potentiated synapses, as well as enhancing hippocampal late-phase LTP and long-term spatial memory. Conditional Fxr1p knockout in mouse forebrain; RNA immunoprecipitation (RIP) for GluA2 mRNA binding; de novo protein synthesis assays; electrophysiology Cell reports High 25456134
2015 Activity-dependent ubiquitination of GluA2 occurs at Lys-870 and Lys-882 in the C-terminal domain, exclusively on plasma membrane AMPARs post-endocytosis, in a Ca2+- and CaMKII-dependent manner requiring L-type VGCCs. Mutation of these lysines does not affect surface expression or AMPA-induced internalization but reduces trafficking to late endosomes and lysosomal degradation. Site-directed mutagenesis of GluA2 ubiquitination sites; Ca2+/CaMKII pathway inhibitors; late endosome co-localization; immunoprecipitation in cultured neurons Cell reports High 25660027
2015 RAB39B, a small GTPase mutated in intellectual disability, controls GluA2 surface expression by acting through PICK1 (a downstream effector of GTP-bound RAB39B); RAB39B-PICK1 controls trafficking from the ER to the Golgi and hence surface expression of GluA2. RAB39B downregulation shifts AMPAR composition toward non-GluA2-containing Ca2+-permeable forms in hippocampal neurons. Co-immunoprecipitation (RAB39B-PICK1); surface GluA2 biochemistry; electrophysiology; RAB39B knockdown in mouse hippocampal neurons Nature communications High 25784538
2015 N-glycosylation at N370 of GluA2 is required for intracellular trafficking from the ER; the N370S mutation strongly suppresses ER exit of GluA2 and co-expressed GluA1. N-glycan at N413 carries the HNK-1 epitope that promotes GluA2 interaction with N-cadherin and enhances cell surface expression of both GluA2 and GluA1. N-glycosylation site mutants expressed in HEK293 cells; ER retention assays; co-immunoprecipitation; surface expression quantification PLoS ONE Medium 26271046
2015 VAMP2 (synaptobrevin-2)-containing postsynaptic vesicles carry GluA1 but not GluA2 in dendritic spines; VAMP2 disruption by tetanus toxin reduces GluA1 in the postsynaptic plasma membrane. GluA1/VAMP2 vesicles are concentrated in spines relative to dendrites, whereas GluA2/VAMP2 vesicles are not, indicating distinct vesicular trafficking pathways for GluA1 and GluA2. Electron microscopy of postsynaptic vesicles; tetanus toxin treatment; immunofluorescence colocalization PLoS ONE Medium 26488171
2015 GSK-3β phosphorylates PICK1 at Ser416 in its C-terminal region; this phosphorylation is required for PICK1 interaction with GluA2. The Ser416Ala substitution disrupts GluA2-PICK1 interaction and increases PICK1 membrane clustering, whereas Ser416Glu/Asp (phosphomimetic) retains the interaction. Site-directed mutagenesis; co-immunoprecipitation; imaging of PICK1 clusters in COS-7 cells; GSK-3β kinase assay The Journal of biological chemistry Medium 26472923
2016 Cryo-EM structure of homomeric GluA2 AMPA receptor saturated with TARP γ2 (stargazin) shows four TARPs arranged with 4-fold symmetry around the ion channel domain, making contacts with M1, M2, and M4 transmembrane helices; two pairs of TARPs are positioned near the LBD dimer and dimer-dimer interfaces to modulate LBD clamshell closure and conformational rearrangements during activation and desensitization. Cryo-electron microscopy structure determination of GluA2-TARP γ2 complex Nature High 27368053
2017 The C-terminal domains (CTDs) of endogenous GluA1 and GluA2 are necessary and sufficient to drive NMDA receptor-dependent LTP and LTD, respectively, in hippocampal CA1 neurons, as demonstrated by knock-in mice with exchanged CTDs. The GluA2 CTD is required for LTD but not LTP. Three knock-in mouse lines with exchanged endogenous AMPAR CTDs; LTP and LTD electrophysiology; behavioral assays Nature neuroscience High 29230056
2017 The membrane-proximal carboxy tail of GluA2 is necessary and sufficient for homeostatic synaptic upscaling in hippocampal CA1 pyramidal neurons; a single amino acid in this region is critical for GluA2-dependent AMPAR trafficking during synaptic scaling. Viral rescue in CA1 neurons with GluA2 domain mutants; whole-cell electrophysiology for synaptic scaling PNAS Medium 29180434
2018 Human autoantibodies against GluA2 induce GluA2-containing AMPAR internalization and reduce synaptic GluA2-containing AMPARs, followed by compensatory ryanodine receptor-dependent incorporation of non-GluA2-containing AMPARs; this disrupts LTP in vitro and impairs learning and memory in vivo. Electrophysiology, high-resolution imaging in neuronal cultures; passive transfer in wild-type and GluA1 KO mice; ryanodine receptor pharmacology Neuron High 30146304
2018 In vivo expression of unedited (Ca2+-permeable) or pore-dead GluA2 in oligodendrocyte precursor cells (OPCs) triggers OPC proliferation and reduces differentiation into oligodendrocytes; expression of the GluA2 C-tail alone decreases OPC differentiation without affecting proliferation, demonstrating separable ionotropic and non-ionotropic roles of GluA2 in OPC fate. In vivo viral expression of GluA2 variants in mouse corpus callosum OPCs; immunohistochemical quantification of OPC proliferation and differentiation Cell reports Medium 30355492
2019 De novo heterozygous GRIA2 mutations causing neurodevelopmental disorders produce a decrease in agonist-evoked current mediated by mutant subunits compared to wild-type; when co-expressed with GluA1, most mutations cause decreased current amplitude and some affect voltage rectification, demonstrating loss-of-function as the principal pathogenic mechanism. Functional expression of mutant GluA2 subunits with electrophysiology in heterologous expression system; co-expression with GluA1 Nature communications High 31300657
2019 FUS/TLS undergoes calcium-dependent nuclear-to-cytoplasmic translocation during excitotoxic stress in neurons; FUS expression is required for glutamate-induced upregulation of GRIA2 mRNA, placing FUS upstream of GluA2 in the excitotoxic stress response. Primary cortical and motor neuron imaging; Ca2+ chelation; FUS knockdown; GRIA2 mRNA quantification in response to glutamate The Journal of biological chemistry Medium 31092554
2020 GluA2 phospho-Y876 is essential for homeostatic synaptic upscaling but not for Hebbian LTP/LTD; bidirectional changes in Y876 phosphorylation occur during scaling (decrease during downscaling, increase during upscaling). Phospho-Y876 is required for synaptic accumulation of GRIP1 during upscaling, and increased Y876 phosphorylation enhances GluA2 binding to GRIP1. GluA2 Y876F phospho-deficient knock-in mice; in vitro and in vivo homeostatic scaling assays; co-immunoprecipitation of GluA2-GRIP1 PNAS High 32071234
2021 RAB39B controls AMPAR trafficking (specifically GluA2/GluA3) to determine dendritic spine maturation; loss of RAB39B in knockout mice increases Ca2+-permeable AMPAR synaptic expression (immature spines), which is rescued by the CP-AMPAR antagonist NASPM, confirming that RAB39B-dependent GluA2 trafficking underlies dendritic spine refinement. Rab39b knockout mouse; spine morphology analysis; electrophysiology; CP-AMPAR pharmacological rescue with NASPM Molecular psychiatry High 34035473
2022 A novel gain-of-function de novo GRIA2 missense mutation (A643V) causes greatly slowed deactivation, markedly reduced desensitization, and increased glutamate sensitivity in GluA2 A643V-containing AMPARs; these gain-of-function properties are distinct from the typical GRIA2 loss-of-function and are fully blocked by perampanel (an AMPAR negative allosteric modulator). Patch-clamp recordings of mutant receptor expressed in HEK293 cells with and without TARP γ2; pharmacological testing with perampanel Epilepsia High 36161652
2025 GluA2-containing AMPARs form a continuum of polyamine-insensitive ion channels with varying degrees of Ca2+ permeability, not a binary Ca2+-impermeable channel as previously held. Ca2+ permeability is shaped by AMPAR subunit composition and by auxiliary subunits (TARPs and cornichons) that primarily modify the selectivity filter; Ca2+ docks at an extracellular binding site that funnels divalent ions into the pore. Patch-clamp electrophysiology with diverse AMPAR subunit combinations and auxiliary subunits; Ca2+ permeability measurements; pharmacological characterization Nature High 40108453

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1993 RNA editing of AMPA receptor subunit GluR-B: a base-paired intron-exon structure determines position and efficiency. Cell 544 8269514
1994 Differences in Ca2+ permeability of AMPA-type glutamate receptor channels in neocortical neurons caused by differential GluR-B subunit expression. Neuron 520 8011338
1995 Early-onset epilepsy and postnatal lethality associated with an editing-deficient GluR-B allele in mice. Science (New York, N.Y.) 474 7502080
1997 The GluR2 (GluR-B) hypothesis: Ca(2+)-permeable AMPA receptors in neurological disorders. Trends in neurosciences 461 9347614
2001 Underediting of glutamate receptor GluR-B mRNA in malignant gliomas. Proceedings of the National Academy of Sciences of the United States of America 317 11717408
1999 Neurological dysfunctions in mice expressing different levels of the Q/R site-unedited AMPAR subunit GluR-B. Nature neuroscience 217 10195181
2019 AMPA receptor GluA2 subunit defects are a cause of neurodevelopmental disorders. Nature communications 201 31300657
1993 Alterations of the GluR-B AMPA receptor subunit flip/flop expression in kainate-induced epilepsy and ischemia. Neuroscience 182 8309523
2014 Structure and dynamics of AMPA receptor GluA2 in resting, pre-open, and desensitized states. Cell 173 25109876
2004 The AMPA receptor subunits GluR-A and GluR-B reciprocally modulate spinal synaptic plasticity and inflammatory pain. Neuron 170 15541312
2011 Retrieval-specific endocytosis of GluA2-AMPARs underlies adaptive reconsolidation of contextual fear. Nature neuroscience 166 21909089
2017 The C-terminal tails of endogenous GluA1 and GluA2 differentially contribute to hippocampal synaptic plasticity and learning. Nature neuroscience 108 29230056
2015 Activity-Dependent Ubiquitination of GluA1 and GluA2 Regulates AMPA Receptor Intracellular Sorting and Degradation. Cell reports 108 25660027
2014 Hippocampus-specific deficiency in RNA editing of GluA2 in Alzheimer's disease. Neurobiology of aging 103 24679603
2014 O-GlcNAcylation of AMPA receptor GluA2 is associated with a novel form of long-term depression at hippocampal synapses. The Journal of neuroscience : the official journal of the Society for Neuroscience 100 24381264
2016 Architecture of fully occupied GluA2 AMPA receptor-TARP complex elucidated by cryo-EM. Nature 97 27368053
2018 Human Autoantibodies against the AMPA Receptor Subunit GluA2 Induce Receptor Reorganization and Memory Dysfunction. Neuron 95 30146304
1994 The organization of the gene for the functionally dominant alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor subunit GluR-B. The Journal of biological chemistry 93 7545935
1995 Editing of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor GluR-B pre-mRNA in vitro reveals site-selective adenosine to inosine conversion. The Journal of biological chemistry 90 7721757
2018 In Vivo Regulation of Oligodendrocyte Precursor Cell Proliferation and Differentiation by the AMPA-Receptor Subunit GluA2. Cell reports 88 30355492
2011 Activity-dependent ubiquitination of the AMPA receptor subunit GluA2. The Journal of neuroscience : the official journal of the Society for Neuroscience 80 21414928
2015 The intellectual disability protein RAB39B selectively regulates GluA2 trafficking to determine synaptic AMPAR composition. Nature communications 78 25784538
1996 Editing of the GLuR-B ion channel RNA in vitro by recombinant double-stranded RNA adenosine deaminase. The EMBO journal 76 8598204
2011 Gain-of-function glutamate receptor interacting protein 1 variants alter GluA2 recycling and surface distribution in patients with autism. Proceedings of the National Academy of Sciences of the United States of America 75 21383172
1998 The AMPA receptor subunit GluR-B in its Q/R site-unedited form is not essential for brain development and function. Proceedings of the National Academy of Sciences of the United States of America 75 9811877
2011 GluA2 (GluR2) regulates metabotropic glutamate receptor-dependent long-term depression through N-cadherin-dependent and cofilin-mediated actin reorganization. The Journal of neuroscience : the official journal of the Society for Neuroscience 73 21248105
2010 Plasma membrane insertion of the AMPA receptor GluA2 subunit is regulated by NSF binding and Q/R editing of the ion pore. Proceedings of the National Academy of Sciences of the United States of America 72 20534470
2010 Lessons from more than 80 structures of the GluA2 ligand-binding domain in complex with agonists, antagonists and allosteric modulators. Neuropharmacology 72 20713069
2013 The molecular link between inefficient GluA2 Q/R site-RNA editing and TDP-43 pathology in motor neurons of sporadic amyotrophic lateral sclerosis patients. Brain research 68 24355598
2003 Glutamatergic plasticity by synaptic delivery of GluR-B(long)-containing AMPA receptors. Neuron 67 14687553
2012 β3 integrin interacts directly with GluA2 AMPA receptor subunit and regulates AMPA receptor expression in hippocampal neurons. Proceedings of the National Academy of Sciences of the United States of America 65 22232691
2000 In vitro analysis of the binding of ADAR2 to the pre-mRNA encoding the GluR-B R/G site. RNA (New York, N.Y.) 64 10836790
2012 Synaptic distributions of GluA2 and PKMζ in the monkey dentate gyrus and their relationships with aging and memory. The Journal of neuroscience : the official journal of the Society for Neuroscience 60 22623679
2010 Plk2 attachment to NSF induces homeostatic removal of GluA2 during chronic overexcitation. Nature neuroscience 60 20802490
2009 Roles of the AMPA receptor subunit GluA1 but not GluA2 in synaptic potentiation and activation of ERK in the anterior cingulate cortex. Molecular pain 60 19664265
1996 Characterization of the ligand-binding domains of glutamate receptor (GluR)-B and GluR-D subunits expressed in Escherichia coli as periplasmic proteins. The Journal of biological chemistry 59 8663017
2013 GluA2-dependent AMPA receptor endocytosis and the decay of early and late long-term potentiation: possible mechanisms for forgetting of short- and long-term memories. Philosophical transactions of the Royal Society of London. Series B, Biological sciences 57 24298143
2012 PICK1 mediates transient synaptic expression of GluA2-lacking AMPA receptors during glycine-induced AMPA receptor trafficking. The Journal of neuroscience : the official journal of the Society for Neuroscience 57 22915106
2000 Analysis of the RNA-editing reaction of ADAR2 with structural and fluorescent analogues of the GluR-B R/G editing site. Biochemistry 55 11015203
2020 A new mouse line with reduced GluA2 Q/R site RNA editing exhibits loss of dendritic spines, hippocampal CA1-neuron loss, learning and memory impairments and NMDA receptor-independent seizure vulnerability. Molecular brain 53 32102661
2013 AMPA receptor pHluorin-GluA2 reports NMDA receptor-induced intracellular acidification in hippocampal neurons. Proceedings of the National Academy of Sciences of the United States of America 53 23940334
2003 Involvement of AMPA receptor GluR2 subunits in stimulus-reward learning: evidence from glutamate receptor gria2 knock-out mice. The Journal of neuroscience : the official journal of the Society for Neuroscience 53 14573529
2014 Prolonged adenosine A1 receptor activation in hypoxia and pial vessel disruption focal cortical ischemia facilitates clathrin-mediated AMPA receptor endocytosis and long-lasting synaptic inhibition in rat hippocampal CA3-CA1 synapses: differential regulation of GluA2 and GluA1 subunits by p38 MAPK and JNK. The Journal of neuroscience : the official journal of the Society for Neuroscience 52 25031403
2001 First images of a glutamate receptor ion channel: oligomeric state and molecular dimensions of GluRB homomers. Biochemistry 49 11705385
2012 S-SCAM/MAGI-2 is an essential synaptic scaffolding molecule for the GluA2-containing maintenance pool of AMPA receptors. The Journal of neuroscience : the official journal of the Society for Neuroscience 48 22593065
2014 GluA2 mRNA distribution and regulation by miR-124 in hippocampal neurons. Molecular and cellular neurosciences 45 24784359
2013 Nerve injury increases GluA2-lacking AMPA receptor prevalence in spinal cords: functional significance and signaling mechanisms. The Journal of pharmacology and experimental therapeutics 45 24030012
2004 Effects of deletion of gria1 or gria2 genes encoding glutamatergic AMPA-receptor subunits on place preference conditioning in mice. Psychopharmacology 45 15619119
1994 Microzonal decreases in the immunostaining for non-NMDA ionotropic excitatory amino acid receptor subunits GluR 2/3 and GluR 5/6/7 in the human epileptogenic neocortex. Brain research 45 7820613
2012 GluA2-lacking AMPA receptors in hippocampal CA1 cell synapses: evidence from gene-targeted mice. Frontiers in molecular neuroscience 44 22375105
2019 MicroRNA-186-5p controls GluA2 surface expression and synaptic scaling in hippocampal neurons. Proceedings of the National Academy of Sciences of the United States of America 43 30808806
2018 Hyperammonemia alters membrane expression of GluA1 and GluA2 subunits of AMPA receptors in hippocampus by enhancing activation of the IL-1 receptor: underlying mechanisms. Journal of neuroinflammation 41 29422059
2014 ADAR2-dependent GluA2 editing regulates cocaine seeking. Molecular psychiatry 40 25349168
2014 Plexin-A4-dependent retrograde semaphorin 3A signalling regulates the dendritic localization of GluA2-containing AMPA receptors. Nature communications 39 24599038
2012 Identification of differentially expressed genes according to chemosensitivity in advanced ovarian serous adenocarcinomas: expression of GRIA2 predicts better survival. British journal of cancer 39 22644307
2007 The C-terminal domain of RNA Pol II helps ensure that editing precedes splicing of the GluR-B transcript. RNA (New York, N.Y.) 39 17525170
1994 Differential RNA editing efficiency of AMPA receptor subunit GluR-2 in human brain. Neuroreport 39 7529592
2014 Trafficking of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA) receptor subunit GluA2 from the endoplasmic reticulum is stimulated by a complex containing Ca2+/calmodulin-activated kinase II (CaMKII) and PICK1 protein and by release of Ca2+ from internal stores. The Journal of biological chemistry 38 24831007
2002 Adenosine to inosine editing by ADAR2 requires formation of a ternary complex on the GluR-B R/G site. The Journal of biological chemistry 37 12163487
2018 A Regulatory Circuitry Between Gria2, miR-409, and miR-495 Is Affected by ALS FUS Mutation in ESC-Derived Motor Neurons. Molecular neurobiology 36 29430619
2015 Postsynaptic VAMP/Synaptobrevin Facilitates Differential Vesicle Trafficking of GluA1 and GluA2 AMPA Receptor Subunits. PloS one 36 26488171
2014 FXR1P limits long-term memory, long-lasting synaptic potentiation, and de novo GluA2 translation. Cell reports 36 25456134
2013 Glutamatergic receptors at developing synapses: the role of GluN3A-containing NMDA receptors and GluA2-lacking AMPA receptors. European journal of pharmacology 35 23872415
2013 Expression, subunit composition, and function of AMPA-type glutamate receptors are changed in activated microglia; possible contribution of GluA2 (GluR-B)-deficiency under pathological conditions. Glia 34 23468421
2012 Thermodynamics and structural analysis of positive allosteric modulation of the ionotropic glutamate receptor GluA2. The Biochemical journal 34 21895609
2017 Estradiol rapidly increases GluA2-mushroom spines and decreases GluA2-filopodia spines in hippocampus CA1. Hippocampus 32 28833901
2019 Neurite-Enriched MicroRNA-218 Stimulates Translation of the GluA2 Subunit and Increases Excitatory Synaptic Strength. Molecular neurobiology 31 30671783
2013 Synthesis, pharmacological and structural characterization, and thermodynamic aspects of GluA2-positive allosteric modulators with a 3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide scaffold. Journal of medicinal chemistry 30 24131202
2011 Structural and functional analysis of two new positive allosteric modulators of GluA2 desensitization and deactivation. Molecular pharmacology 30 21543522
2020 Tyrosine phosphorylation of the AMPA receptor subunit GluA2 gates homeostatic synaptic plasticity. Proceedings of the National Academy of Sciences of the United States of America 29 32071234
2017 Synaptic homeostasis requires the membrane-proximal carboxy tail of GluA2. Proceedings of the National Academy of Sciences of the United States of America 29 29180434
2015 Glycogen Synthase Kinase 3β-mediated Phosphorylation in the Most C-terminal Region of Protein Interacting with C Kinase 1 (PICK1) Regulates the Binding of PICK1 to Glutamate Receptor Subunit GluA2. The Journal of biological chemistry 29 26472923
2023 The Q/R editing site of AMPA receptor GluA2 subunit acts as an epigenetic switch regulating dendritic spines, neurodegeneration and cognitive deficits in Alzheimer's disease. Molecular neurodegeneration 28 37759260
2017 Adaptor Complex 2 Controls Dendrite Morphology via mTOR-Dependent Expression of GluA2. Molecular neurobiology 28 28190237
2015 GluA2 is rapidly edited at the Q/R site during neural differentiation in vitro. Frontiers in cellular neuroscience 28 25798088
1997 Distribution of glutamate receptors GluR 2/3 and NR1 in the developing rat cerebellum. Neuroscience 28 9300432
2021 A circuit of mossy cells controls the efficacy of memory retrieval by Gria2I inhibition of Gria2. Cell reports 27 33596426
2021 GluA2 overexpression in oligodendrocyte progenitors promotes postinjury oligodendrocyte regeneration. Cell reports 27 34010640
2019 The RNA-binding protein FUS/TLS undergoes calcium-mediated nuclear egress during excitotoxic stress and is required for GRIA2 mRNA processing. The Journal of biological chemistry 27 31092554
2019 D-Asp upregulates PREP and GluA2/3 expressions and induces p-ERK1/2 and p-Akt in rat testis. Reproduction (Cambridge, England) 27 31398714
2017 Endocytosis and lysosomal degradation of GluA2/3 AMPARs in response to oxygen/glucose deprivation in hippocampal but not cortical neurons. Scientific reports 27 28951554
2015 Environmental Enrichment Increases Glucocorticoid Receptors and Decreases GluA2 and Protein Kinase M Zeta (PKMζ) Trafficking During Chronic Stress: A Protective Mechanism? Frontiers in behavioral neuroscience 27 26617502
2008 Study on GRIA2, GRIA3 and GRIA4 genes highlights a positive association between schizophrenia and GRIA3 in female patients. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 27 18163426
2001 Q/R RNA editing of the AMPA receptor subunit 2 (GRIA2) transcript evolves no later than the appearance of cartilaginous fishes. FEBS letters 26 11741603
2016 miR-181a is a negative regulator of GRIA2 in methamphetamine-use disorder. Scientific reports 24 27767084
2018 M1 muscarinic receptors facilitate hippocampus-dependent cognitive flexibility via modulating GluA2 subunit of AMPA receptors. Neuropharmacology 23 30529302
2025 GluA2-containing AMPA receptors form a continuum of Ca2+-permeable channels. Nature 22 40108453
2012 Partial deletion of GLRB and GRIA2 in a patient with intellectual disability. European journal of human genetics : EJHG 22 22669415
2022 GluA2-lacking AMPA receptors in the nucleus accumbens core and shell contribute to the incubation of oxycodone craving in male rats. Addiction biology 21 36301206
2022 A gain-of-function GRIA2 variant associated with neurodevelopmental delay and seizures: Functional characterization and targeted treatment. Epilepsia 20 36161652
2017 PICK1 facilitates lasting reduction in GluA2 concentration in the hippocampus during chronic epilepsy. Epilepsy research 20 28888867
2015 Role of Site-Specific N-Glycans Expressed on GluA2 in the Regulation of Cell Surface Expression of AMPA-Type Glutamate Receptors. PloS one 20 26271046
2020 Expansion of the GRIA2 phenotypic representation: a novel de novo loss of function mutation in a case with childhood onset schizophrenia. Journal of human genetics 19 32948840
2014 Specificity protein 4 (Sp4) regulates the transcription of AMPA receptor subunit GluA2 (Gria2). Biochimica et biophysica acta 19 24576410
2020 Transient Enhanced GluA2 Expression in Young Hippocampal Neurons of a Fragile X Mouse Model. Frontiers in synaptic neuroscience 18 33343326
2004 Tra2betal regulates P19 neuronal differentiation and the splicing of FGF-2R and GluR-B minigenes. Cell biology international 18 15563401
2021 RAB39B-mediated trafficking of the GluA2-AMPAR subunit controls dendritic spine maturation and intellectual disability-related behaviour. Molecular psychiatry 17 34035473
2019 Vascular endothelial growth factor increases the function of calcium-impermeable AMPA receptor GluA2 subunit in astrocytes via activation of protein kinase C signaling pathway. Glia 17 30883902
2018 Distinct Roles of GluA2-lacking AMPA Receptor Expression in Dopamine D1 or D2 Receptor Neurons in Animal Behavior. Neuroscience 17 30537522
2013 Evaluation of PhTX-74 as subtype-selective inhibitor of GluA2-containing AMPA receptors. Molecular pharmacology 17 24220009

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