Affinage

GRIA4

Glutamate receptor 4 · UniProt P48058

Length
902 aa
Mass
100.9 kDa
Annotated
2026-06-10
44 papers in source corpus 24 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GRIA4 encodes GluA4 (GluR-D), an AMPA-type ionotropic glutamate receptor subunit that supplies fast-kinetic excitatory transmission at defined central synapses and governs activity-dependent synaptic strengthening during development (PMID:24599589, PMID:21857658, PMID:18316356). Its extracellular S1S2 ligand-binding domain folds into an autonomous module that binds AMPA with ~60 nM affinity independently of glycosylation, stabilized by a buried C260–C315 disulfide bond, with R507 and E727 forming ion-pair contacts that are selectively required for agonist over antagonist engagement and helix-F residues (L672, T677) tuning agonist affinity (PMID:8663017, PMID:9737972, PMID:12167621, PMID:12473122). The N-terminal domain mediates subunit dimerization without contributing to ligand binding (PMID:10506139), and cryo-EM resolves a Y-shaped, domain-swapped architecture in which glutamate-saturated LBDs gate the channel through asymmetric hinging, with conformational plasticity underlying subconductance states; an LBD regulatory site for the auxiliary subunit TARP-γ2 slows channel opening and closing and tunes desensitization across the gating cycle (PMID:40954371, PMID:40667226, PMID:41656278, PMID:31267004). Surface delivery depends on a 14-residue C-terminal cytoplasmic segment that binds 4.1-family proteins, while a terminal proline blocks canonical PDZ binding to SAP97 (PMID:12574408, PMID:20090852); at immature hippocampal synapses, PKA drives synaptic insertion of GluA4 through an intramolecular C-terminal mechanism that defines neonatal PKA-dependent LTP and the maturation of glutamatergic circuitry (PMID:24599589, PMID:27157711). At the circuit level GluA4 sets EPSC speed and amplitude at corticothalamic reticular, cerebellar mossy fiber–granule cell, and auditory brainstem synapses, where its loss impairs spike fidelity, associative eyeblink memory, and corticothalamic drive, and Gria4 disruption produces absence seizures (PMID:21857658, PMID:18316356, PMID:34219651, PMID:26390982). De novo variants in the M3 SYTANLAAF gating motif of GRIA4 cause intellectual disability with or without seizures (PMID:29220673).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1996 High

    Establishing that the isolated S1S2 segment is a self-contained ligand-binding module answered whether the AMPA binding site could fold without the rest of the receptor and without glycosylation.

    Evidence bacterial periplasmic expression of S1S2 with [3H]AMPA binding and deletion mutagenesis

    PMID:8663017

    Open questions at the time
    • Does not resolve how the LBD couples to channel gating
    • flip/flop functional consequences beyond equal binding affinity not addressed
  2. 1998 High

    Identifying the C260–C315 disulfide as essential for LBD stability explained why correct folding and ligand-binding competence depend on a specific intradomain bond.

    Evidence biochemical disulfide analysis with C260S/C315S mutagenesis and [3H]AMPA binding

    PMID:9737972

    Open questions at the time
    • Effect on full channel gating not measured
    • redox regulation in vivo unaddressed
  3. 1999 Medium

    Showing the N-terminal X domain dimerizes while S1S2 stays monomeric localized subunit-assembly contacts to the extracellular N-terminus.

    Evidence hydrodynamic analysis of recombinant domain fragments with radioligand binding

    PMID:10506139

    Open questions at the time
    • In vitro fragment behavior, not full receptor assembly
    • single lab
  4. 2002 High

    Pinpointing R507, E727, and helix-F residues distinguished agonist from antagonist binding determinants, dissecting how the LBD discriminates activating from blocking ligands.

    Evidence site-directed mutagenesis with multiple radioligand binding assays and ligand docking

    PMID:12167621 PMID:12473122

    Open questions at the time
    • Binding determinants mapped, but link to gating kinetics not measured directly
  5. 2003 High

    Mapping a 14-residue C-terminal segment that binds 4.1 proteins answered how GluA4 reaches and is retained at the cell surface.

    Evidence C-terminal deletion, co-IP and GST pull-down in HEK293 and brain, surface ELISA, point mutagenesis

    PMID:12574408

    Open questions at the time
    • Identity of the specific 4.1 family member at synapses not resolved
    • structural basis of the interaction unknown
  6. 2008 High

    Genetic complementation linking Gria4 loss to spike-wave discharges established GluA4 as a fast AMPA subunit whose absence dysregulates reticular thalamic excitation and causes absence seizures.

    Evidence EEG, complementation test, Gria4 and Gria3 knockout mice, electrophysiology

    PMID:18316356

    Open questions at the time
    • Molecular basis of prolonged synaptic responses beyond loss of a fast subunit not fully resolved
  7. 2010 High

    Demonstrating that a terminal proline blocks SAP97 binding clarified why GluA4 does not engage canonical PDZ scaffolds despite a class-I-like C-terminus.

    Evidence reciprocal co-IP and mass spectrometry in cells and mouse brain with proline-deletion constructs

    PMID:20090852

    Open questions at the time
    • Whether any physiological condition relieves this block unaddressed
  8. 2014 High

    Showing GluA4 defines a PKA-dependent neonatal form of LTP and is required at the cortico-nRT projection connected molecular trafficking to developmental and circuit-level functions.

    Evidence LTP recordings, Gria4 knockout, lentiviral GluA4 expression, PKA pharmacology, optogenetics

    PMID:21857658 PMID:24599589

    Open questions at the time
    • Molecular identity of the PKA-driven trafficking step not yet defined here
    • downstream effectors of GluA4 mobilization unclear
  9. 2016 Medium

    Identifying an intramolecular C-terminal interaction controlling PKA-driven insertion defined the molecular switch for GluA4 synaptic delivery and synapse maturation.

    Evidence electrophysiology with C-terminal deletion/mutation constructs and Gria4 knockout mice

    PMID:27157711

    Open questions at the time
    • Structural model of the intramolecular contact not resolved
    • single lab
  10. 2017 Medium

    Quantitative kinetic and structural studies of TARP modulation established how auxiliary subunits tune GluA4 gating, and scaffold/co-IP work linked GluA4 delivery to SAP97-KSR1/PKC complexes during conditioning.

    Evidence freeze-fracture immunogold localization, laser-pulse photolysis kinetics, co-IP in conditioning models

    PMID:24567325 PMID:28397107

    Open questions at the time
    • SAP97 complex evidence is co-IP based without reciprocal in vivo validation
    • TARP isoform specificity in vivo incompletely mapped
  11. 2017 Low

    Identifying de novo SYTANLAAF (M3) variants linked GRIA4 to intellectual disability with or without seizures, implicating gating disruption in disease.

    Evidence trio whole-exome sequencing with molecular modeling of the gating motif

    PMID:29220673

    Open questions at the time
    • No direct functional validation of the predicted gating defects in this study
    • genotype-phenotype mechanism inferred computationally
  12. 2021 High

    Demonstrating an ~80% loss of mossy fiber–granule cell transmission and failed associative memory in knockouts established GluA4 as essential for cerebellar input fidelity and learning.

    Evidence electrophysiology, computational modeling, and delay eyeblink conditioning in GluA4 knockout mice

    PMID:34219651

    Open questions at the time
    • Compensatory NMDAR/tonic inhibition changes complicate isolating GluA4-specific contribution
  13. 2025 High

    Full gating-cycle cryo-EM structures with TARP-γ2 and single-channel recordings provided the structural basis for asymmetric LBD-driven gating, subconductance states, and a TARP regulatory site.

    Evidence cryo-EM in active/resting/desensitized states and single-channel bilayer recordings

    PMID:40667226 PMID:40954371 PMID:41656278

    Open questions at the time
    • Structures of heteromeric native GluA4 receptors not resolved
    • structural correlates of C-terminal trafficking interactions absent

Open questions

Synthesis pass · forward-looking unresolved questions
  • How GluA4's intracellular trafficking machinery (4.1 binding, intramolecular C-terminal switch, PKA phosphorylation) maps onto its resolved channel structure and onto heteromeric native assemblies remains unresolved.
  • No structure of the GluA4 cytoplasmic domain or its scaffold interactions
  • native subunit composition at each synapse type not structurally defined
  • in vivo phosphosite-level regulation of trafficking unmapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Localization
GO:0005886 plasma membrane 2
Pathway
R-HSA-112316 Neuronal System 3
Partners
CACNG2CACNG4DLG1EPB41
Complex memberships
AMPA receptorGluA4:TARP-γ2 complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2025 Cryo-EM structures of rat GluA4:TARP-γ2 were solved in active, resting, and desensitized states, covering a full gating cycle. GluA4 alone displays a classical Y-shaped conformation. In resting conditions, GluA4:TARP-γ2 adopts two conformations, one resembling the desensitized state. A regulatory site for TARP-γ2 was identified in the ligand-binding domain that modulates gating kinetics. Cryo-electron microscopy (cryo-EM) structural determination with functional validation Nature structural & molecular biology High 40954371
2025 Cryo-EM structures of GluA4 AMPARs reveal a canonical Y-shaped architecture with domain-swapping between ATD and LBD. All four LBDs can be glutamate-bound yet open the ion channel by asymmetric hinging in all channel helices. Conformational plasticity of the glutamate-saturated LBD tunes the ion channel gate, providing a structural basis for subconductance states. Cryo-electron microscopy (cryo-EM) and single-channel bilayer recordings bioRxiv (preprint) / Nature communicationspreprint High 40667226 41656278
2003 Surface expression of homomeric GluA4 (GluR-D) AMPA receptors requires a 14-residue cytoplasmic C-terminal segment that mediates binding to 4.1 family proteins. Co-immunoprecipitation demonstrated GluA4 associates with 4.1 protein(s) in both HEK293 cells and rat brain. GST pull-down confirmed the same segment is critical for 4.1 binding. Point mutations within this segment dramatically decreased surface expression with concomitant loss of 4.1 interaction. C-terminal deletion analysis, co-immunoprecipitation, GST pull-down, immunofluorescence/ELISA surface expression assay, point mutagenesis The Journal of neuroscience High 12574408
1999 The N-terminal X domain of GluA4 (GluRD) forms dimers in solution (shown by hydrodynamic analysis of recombinant fragments), whereas the S1S2 ligand-binding domain is monomeric. The X domain does not bind AMPA or glutamate, nor affect ligand binding properties of the S1S2 domain. This suggests subunit-subunit interactions in AMPA receptors involve the extracellular N-terminal domain. Recombinant protein expression in insect cells, hydrodynamic analysis, [3H]AMPA/glutamate radioligand binding assays The Journal of biological chemistry Medium 10506139
1996 The S1-S2 ligand-binding domain of GluA4 (GluR-D) expressed in E. coli as a soluble periplasmic protein bound [3H]AMPA with high affinity (Kd = 60 nM) and pharmacology typical of native AMPA receptors, demonstrating N-linked glycosylation is not required for ligand-binding site formation. The flip and flop splice variants bind [3H]AMPA with equal affinity; deletion of the C-terminal one-third of S2 abolished binding activity. Bacterial periplasmic expression, [3H]AMPA radioligand binding assays, deletion mutagenesis The Journal of biological chemistry High 8663017
1998 A disulfide bond exists in the ligand-binding domain of GluA4 (GluRD) between conserved cysteines C260 and C315, but is inaccessible to DTT in the intact receptor. Single mutants C260S and C315S show 2-3-fold higher ligand affinity than wild-type. Mutants lacking the native disulfide show non-native oligomerization and dramatically reduced specific activity, indicating the disulfide is required for ligand-binding domain stability. Biochemical disulfide analysis, site-directed mutagenesis, [3H]AMPA binding assays The Journal of biological chemistry High 9737972
2002 Site-directed mutagenesis of the helix F region of GluA4 (GluR-D) ligand-binding domain showed that L672 and T677 alanine substitutions severely reduced affinity for all agonists, while mutations at D673, S674, G675, S676, and K678 selectively affected specific agonists. Strikingly, antagonist binding affinities (Ro 48-8587, DNQX) were unaffected by all these mutations, demonstrating selective engagement of helix F side chains in agonist but not antagonist binding. Site-directed mutagenesis, radioligand binding assays ([3H]AMPA, [3H]Ro 48-8587), ligand docking The Journal of biological chemistry High 12167621
2002 R507 in GluA4 (GluR-D) is essential for both agonist and antagonist binding (even conservative R507K abolishes binding). E727 is required for agonist binding via ion-pair interaction; the isosteric E727Q mutation abolished all agonist binding but retained high-affinity antagonist binding, indicating that E727 ion-pair interaction is selectively required for agonist activity. Site-directed mutagenesis, [3H]AMPA and [3H]Ro 48-8587 radioligand binding assays, competition binding, ligand docking European journal of biochemistry High 12473122
2010 Native GluA4 receptors contain a C-terminal proline that blocks canonical PDZ interactions. Deletion of this proline conferred avid binding to SAP97 in cultured cells by co-immunoprecipitation, whereas wild-type GluA4 did not associate with SAP97. Mass spectrometry confirmed that native GluA4 C-terminus is intact and the single-residue cleavage does not occur to a significant extent in vivo. Co-immunoprecipitation, mass spectrometry, antibody generation against proline-deleted GluA4 C-terminus PloS one High 20090852
2014 GluA4 expression in immature CA1 pyramidal neurons is sufficient to alter LTP signaling requirements. At immature synapses, PKA activation leads to synaptic potentiation via GluA4 mobilization. GluA4-deficient mice lack neonatal PKA-dependent LTP. Lentiviral expression of GluA4 in CA1 neurons at any developmental stage confers PKA-dependent synaptic potentiation and LTP, demonstrating GluA4 defines the switch in LTP kinase dependency from PKA to CaMKII during synapse maturation. Electrophysiology (LTP recordings), GluA4 knockout mice, lentiviral GluA4 overexpression, PKA pharmacology Proceedings of the National Academy of Sciences of the United States of America High 24599589
2016 PKA activation leads to synaptic insertion of GluA4 at initially weak or silent CA1 synapses. This effect depends on a novel mechanism involving the extreme C-terminal end of GluA4, which interacts with the membrane-proximal region of its own C-terminal domain to control GluA4 trafficking. In the absence of GluA4, functional maturation of glutamatergic synapses during postnatal development was significantly delayed. Electrophysiology, C-terminal deletion/mutation constructs, GluA4 knockout mice, PKA pharmacology Neuropharmacology Medium 27157711
2014 GluA4-containing AMPARs in the reticular thalamus mediate cortico-nRT synaptic excitation. In Gria4 knockout mice, synaptic excitation of inhibitory reticular thalamic neurons is specifically reduced at the cortico-nRT projection. Absence seizures (spike-wave discharges) can still be initiated via the cortico-TC-nRT-TC pathway, revealing a bypass mode of corticothalamic transmission. Electrophysiology in Gria4 knockout mice, optogenetic stimulation of corticothalamic pathways PLoS genetics / Nature neuroscience High 18316356 21857658
2008 A hypomorphic retroviral-like insertion in Gria4 causes absence seizures in C3H/HeJ mice. Gria4 knockout mice have frequent spike-wave discharges, and Gria4(-/-) does not complement the spkw1 locus. In contrast, Gria3 null mutants do not have SWD. In Gria4 mutants, synaptic excitation of inhibitory reticular thalamic neurons is enhanced with increased duration of synaptic responses, consistent with reduction of a kinetically fast AMPA receptor subunit. EEG recordings, genetic complementation, Gria4 knockout and Gria3 knockout mice, electrophysiology Human molecular genetics High 18316356
2009 TARPs stargazin (γ2) and γ4 slow desensitization of homomeric GluA4 (GluR-D) AMPA receptors, increasing steady-state current. Ethanol concentration-dependently accelerates the rate of GluA4 desensitization, and this effect is enhanced by TARP coexpression. Recovery from desensitization was slowed by γ4 but ethanol did not affect this process. Whole-cell electrophysiology in HEK293 cells, TARP co-expression, ethanol pharmacology Alcohol (Fayetteville, N.Y.) Medium 19560629
2019 Both stargazin (γ2, type 1a TARP) and γ4 (type 1b TARP) slow the channel-opening rate (kop) and channel-closing rate (kcl) of GluA4 homomeric AMPA receptor channels each by approximately 4-fold and 3-fold respectively, without appreciable change in channel-opening probability. γ4 has a stronger effect on slowing desensitization rate than γ2, while γ2 causes a larger left-shift of the dose-response curve. Laser-pulse photolysis technique for rapid ligand application, single-channel and macroscopic current analysis Scientific reports Medium 31267004
2021 GluA4 knockout in mice reduces mossy fiber to granule cell synaptic transmission by ~80%. Despite compensatory changes (attenuated tonic inhibition, increased NMDAR transmission), granule cell spike output fidelity was markedly decreased. GluA4 knockout mice failed to form associative memories in delay eyeblink conditioning, while locomotor coordination was generally spared. Electrophysiology in GluA4 knockout mice, computational network modeling, behavioral conditioning eLife High 34219651
2013 Repeated morphine administration leads to synaptic insertion of GluA4-containing Ca2+-permeable AMPARs in spinal cord dorsal horn laminae III-V. Co-immunoprecipitation suggested increase in GluA4 homomers. EPSC rectification index increased in morphine-treated mice, and infusion of GluA4 antibody through the patch pipette reversed the enhanced Ca2+-permeable AMPAR-mediated EPSCs. Intrathecal Ca2+-permeable AMPAR blocker disrupted morphine-induced mechanical hypersensitivity. Co-immunoprecipitation, immunohistochemistry, electrophysiology (whole-cell patch clamp, rectification index), intrathecal pharmacology, GluA4 antibody infusion via patch pipette Neuropsychopharmacology High 23403695
2014 Sequential synaptic delivery of GluA4-containing AMPARs during classical conditioning involves SAP97 scaffold. Conditioning induces formation of a SAP97-KSR1/PKC-GluA4 protein complex that delivers GluA4 to the PSD via SAP97-PSD95 interaction. This occurs after an initial PKA-dependent SAP97-AKAP/PKA-GluA1 complex delivers GluA1-containing AMPARs. Co-immunoprecipitation, in vitro eyeblink classical conditioning model, pharmacological inhibitors The Journal of biological chemistry Medium 24567325
2015 Loss of GluA4 at corticothalamic L5B-POm synapses almost abolished EPSC amplitude and strongly delayed onset of action potential generation, demonstrating GluA4 is required to produce an EPSC sufficiently large to trigger postsynaptic action potentials within a defined time window after presynaptic input. Virus-mediated genetic knockdown, whole-cell electrophysiology, direct stimulation of single corticothalamic terminals The European journal of neuroscience Medium 26390982
2016 Acoustic trauma decreases GluA4 mRNA and increases GluA1 mRNA in the lateral superior olive (LSO), slowing AMPAR-EPSC decay times. These changes are reversible within two months. Computational modeling confirmed that longer-lasting EPSCs after GluA4 reduction compensate to maintain binaural function with raised auditory thresholds. Voltage-clamp electrophysiology, mRNA quantification, auditory brainstem responses, computational modeling The Journal of physiology Medium 27104476
2017 Quantitative freeze-fracture replica immunogold labeling of auditory nerve synapses showed higher number and density of GluA4 subunits at auditory nerve to fusiform cell (AN-FC) synapses compared to bushy cell (AN-BC) synapses, while GluA3 is enriched at AN-BC synapses. GluA4 gold labeling was homogeneously distributed along both synapse types, contrasting with the central distribution of GluA3 at AN-BC synapses. Quantitative freeze-fracture replica immunogold labeling (FRIL), GluA3 knockout mice Brain structure & function Medium 28397107
2017 De novo heterozygous variants in the SYTANLAAF motif of GRIA4 transmembrane domain M3 (a conserved gating motif) cause intellectual disability with or without seizures. Molecular modeling showed that three variants orient toward the pore center and are predicted to disturb the gating mechanism; a fourth variant in the same motif likely reduces permeability; a fifth extracellular domain variant potentially interferes with monomer binding. Trio whole-exome sequencing, molecular modeling of gating mechanism American journal of human genetics Low 29220673
2004 Human GluR4c is an alternative splicing isoform of GluA4 with a 113-bp insert containing a stop codon resulting in a short C terminus. Its expression is widespread in the adult human brain and upregulated with development in cerebellum and cerebral cortex, reaching ~30% of total GluA4 mRNA in adults. cDNA cloning, RT-PCR expression profiling Brain research. Molecular brain research Low 15306133

Source papers

Stage 0 corpus · 44 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 A new mode of corticothalamic transmission revealed in the Gria4(-/-) model of absence epilepsy. Nature neuroscience 151 21857658
2003 Surface expression of GluR-D AMPA receptor is dependent on an interaction between its C-terminal domain and a 4.1 protein. The Journal of neuroscience : the official journal of the Society for Neuroscience 83 12574408
1999 Oligomerization and ligand-binding properties of the ectodomain of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor subunit GluRD. The Journal of biological chemistry 79 10506139
2008 Absence seizures in C3H/HeJ and knockout mice caused by mutation of the AMPA receptor subunit Gria4. Human molecular genetics 72 18316356
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
2017 De Novo Variants in GRIA4 Lead to Intellectual Disability with or without Seizures and Gait Abnormalities. American journal of human genetics 54 29220673
2003 Positive association of the AMPA receptor subunit GluR4 gene (GRIA4) haplotype with schizophrenia: linkage disequilibrium mapping using SNPs evenly distributed across the gene region. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 45 12497607
2020 CircCBFB-mediated miR-28-5p facilitates abdominal aortic aneurysm via LYPD3 and GRIA4. Life sciences 42 32151690
1995 Purification of recombinant GluR-D glutamate receptor produced in Sf21 insect cells. European journal of biochemistry 39 8521834
2019 Genes CEP55, FOXD3, FOXF2, GNAO1, GRIA4, and KCNA5 as potential diagnostic biomarkers in colorectal cancer. BMC medical genomics 38 30987631
2016 Acoustic trauma slows AMPA receptor-mediated EPSCs in the auditory brainstem, reducing GluA4 subunit expression as a mechanism to rescue binaural function. The Journal of physiology 30 27104476
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
2017 The number and distribution of AMPA receptor channels containing fast kinetic GluA3 and GluA4 subunits at auditory nerve synapses depend on the target cells. Brain structure & function 26 28397107
2014 Developmental switch in the kinase dependency of long-term potentiation depends on expression of GluA4 subunit-containing AMPA receptors. Proceedings of the National Academy of Sciences of the United States of America 25 24599589
2018 Genome-wide association study identifies glutamate ionotropic receptor GRIA4 as a risk gene for comorbid nicotine dependence and major depression. Translational psychiatry 24 30287806
1998 Disulfide bonding and cysteine accessibility in the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor subunit GluRD. Implications for redox modulation of glutamate receptors. The Journal of biological chemistry 24 9737972
2021 GluA4 facilitates cerebellar expansion coding and enables associative memory formation. eLife 21 34219651
2013 Pain after discontinuation of morphine treatment is associated with synaptic increase of GluA4-containing AMPAR in the dorsal horn of the spinal cord. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 21 23403695
2016 Molecular mechanisms controlling synaptic recruitment of GluA4 subunit-containing AMPA-receptors critical for functional maturation of CA1 glutamatergic synapses. Neuropharmacology 19 27157711
2019 GluA4-Targeted AAV Vectors Deliver Genes Selectively to Interneurons while Relying on the AAV Receptor for Entry. Molecular therapy. Methods & clinical development 18 31463334
2014 Unraveling genetic modifiers in the gria4 mouse model of absence epilepsy. PLoS genetics 18 25010494
2014 Sequential delivery of synaptic GluA1- and GluA4-containing AMPA receptors (AMPARs) by SAP97 anchored protein complexes in classical conditioning. The Journal of biological chemistry 17 24567325
2015 Ionotropic glutamate receptor GluA4 and T-type calcium channel Cav 3.1 subunits control key aspects of synaptic transmission at the mouse L5B-POm giant synapse. The European journal of neuroscience 15 26390982
2016 GluA4 subunit of AMPA receptors mediates the early synaptic response to altered network activity in the developing hippocampus. Journal of neurophysiology 14 26961102
2004 No genetic association between polymorphisms in the AMPA receptor subunit GluR4 gene (GRIA4) and schizophrenia in the Chinese population. Neuroscience letters 13 15450689
2009 Ethanol increases desensitization of recombinant GluR-D AMPA receptor and TARP combinations. Alcohol (Fayetteville, N.Y.) 12 19560629
2021 Role of GluA4 in the acoustic and tactile startle responses. Hearing research 11 34915397
2023 Hypermethylated GRIA4, a potential biomarker for an early non-invasive detection of metastasis of clinically known colorectal cancer. Frontiers in oncology 9 37476382
2022 Novel Heterozygous Missense Variant in GRIA4 Gene Associated With Neurodevelopmental Disorder With or Without Seizures and Gait Abnormalities. Frontiers in genetics 9 35518358
2016 Hippocampal GluA2 and GluA4 protein but not corresponding mRNA and promoter methylation levels are modulated at retrieval in spatial learning of the rat. Amino acids 9 27714514
2004 GluR4c, an alternative splicing isoform of GluR4, is abundantly expressed in the adult human brain. Brain research. Molecular brain research 9 15306133
2013 Genetic analysis of GRIA2 and GRIA4 genes in migraine. Headache 8 24512576
2002 Discrimination between agonists and antagonists by the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid-selective glutamate receptor. A mutation analysis of the ligand-binding domain of GluR-D subunit. The Journal of biological chemistry 8 12167621
2021 Neuronal activity regulated pentraxin (narp) and GluA4 subunit of AMPA receptor may be targets for fluoxetine modulation. Metabolic brain disease 7 33528752
2017 GluA4 Dependent Plasticity Mechanisms Contribute to Developmental Synchronization of the CA3-CA1 Circuitry in the Hippocampus. Neurochemical research 7 28856535
2010 Analysis of the potential role of GluA4 carboxyl-terminus in PDZ interactions. PloS one 7 20090852
2013 Investigation of possible epistatic interactions between GRIA2 and GRIA4 variants on clinical outcomes in patients with major depressive disorder. The Journal of international medical research 6 23613500
2002 Determinants of antagonist binding at the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit, GluR-D. Role of the conserved arginine 507 and glutamate 727 residues. European journal of biochemistry 6 12473122
2025 GluA4 AMPA receptor gating mechanisms and modulation by auxiliary proteins. Nature structural & molecular biology 5 40954371
2019 Stargazin and γ4 slow the channel opening and closing rates of GluA4 AMPA receptors. Scientific reports 5 31267004
2025 Architecture, Activation, and Conformational Plasticity in the GluA4 AMPA Receptor. bioRxiv : the preprint server for biology 3 40667226
2010 Cloning and characterization of glutamate receptor subunit 4 (GLUA4) and its alternatively spliced isoforms in turtle brain. Journal of molecular neuroscience : MN 3 20549383
2026 Structural basis for activation and conformational plasticity of the GluA4 AMPA receptor. Nature communications 1 41656278
2016 A parallel panning scheme used for selection of a GluA4-specific Fab targeting the ligand-binding domain. International journal of biological macromolecules 1 27402461

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