ArticleMolecular brain2012
Direct interaction between GluR2 and GAPDH regulates AMPAR-mediated excitotoxicity.
Article in Molecular brain, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- Distinct Roles of NMDA and AMPA Receptors in the Pathogenesis of Hyperbaric Oxygen-Induced Seizures.Biomedicines · 2026Article
- Review
- Immunoexcitoxicity as the possible major pathophysiology behind multiple sclerosis and other autoimmune disorders.Surgical neurology international · 2025Article
- Novel α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPAR) potentiator LT-102: A promising therapeutic agent for treating cognitive impairment associated with schizophrenia.CNS neuroscience & therapeutics · 2024Article
- Small-molecule targeting AMPA-mediated excitotoxicity has therapeutic effects in mouse models for multiple sclerosis.Science advances · 2023Article
- Development of a novel peptide to prevent entry of SARS-CoV-2 into lung and olfactory bulb cells of hACE2 expressing mice.Molecular brain · 2022Article
- Review
- Constraint-induced movement therapy enhances AMPA receptor-dependent synaptic plasticity in the ipsilateral hemisphere following ischemic stroke.Neural regeneration research · 2021Article
- Targeting redox regulation to treat substance use disorder using N‐acetylcysteineThe European journal of neuroscience · 2019Review
- Long-term depression induced by endogenous cannabinoids produces neuroprotection via astroglial CBJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Glial Cell AMPA Receptors in Nervous System Health, Injury and Disease.International journal of molecular sciences · 2019Review
- Monogenic, Polygenic, and MicroRNA Markers for Ischemic Stroke.Molecular neurobiology · 2019Review
- Phased Treatment Strategies for Cerebral Ischemia Based on Glutamate Receptors.Frontiers in cellular neuroscience · 2019Review
- High Pressure Stress Response: Involvement of NMDA Receptor Subtypes and Molecular Markers.Frontiers in physiology · 2019Article
- Specific Alterations in Astrocyte Properties via the GluA2-GAPDH Complex Associated with Multiple Sclerosis.Scientific reports · 2018Article
- Disrupting GluA2-GAPDH Interaction Affects Axon and Dendrite Development.Scientific reports · 2016Article
- Quantitative proteomics analysis of zebrafish exposed to sub-lethal dosages of β-methyl-amino-L-alanine (BMAA).Scientific reports · 2016Article
- Blocking GluR2-GAPDH ameliorates experimental autoimmune encephalomyelitis.Annals of clinical and translational neurology · 2015Article
- Involvement of GluR2 up-regulation in neuroprotection by electroacupuncture pretreatment via cannabinoid CB1 receptor in mice.Scientific reports · 2015Article
- NMDA glutamate receptor NR1, NR2A and NR2B expression and NR2B Tyr-1472 phosphorylation in the lens.Neurochemical research · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over-activation of AMPARs (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid subtype glutamate receptors) is implicated in excitotoxic neuronal death associated with acute brain insults, such as ischemic stroke. However, the specific molecular mechanism by which AMPARs, especially the calcium-impermeable AMPARs, induce neuronal death remains poorly understood. Here we report the identification of a previously unrecognized molecular pathway involving a direct protein-protein interaction that underlies GluR2-containing AMPAR-mediated excitotoxicity. Agonist stimulation of AMPARs promotes GluR2/GAPDH (glyceraldehyde-3-phosphate dehydrogenase) complex formation and subsequent internalization. Disruption of GluR2/GAPDH interaction by administration of an interfering peptide prevents AMPAR-mediated excitotoxicity and protects against damage induced by oxygen-glucose deprivation (OGD), an in vitro model of brain ischemia.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.