ReviewNeuropharmacology2021
Clinical and therapeutic significance of genetic variation in the GRIN gene family encoding NMDARs.
Review in Neuropharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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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.
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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.
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Who cites it
55 citing papers in PubMed.
- The AMPA receptor life cycle: assembly, regulation and synaptic diversity.Nature reviews. Neuroscience · 2026Review
- State-specific inhibition of NMDA receptors by memantine provides insight into NMDAR channel blocker tolerability.Science advances · 2026Article
- Movement Disorders in Developmental and Epileptic Encephalopathies.Movement disorders clinical practice · 2026Review
- Article
- Inhibition of GluN2B-containing N-methyl-D-aspartate receptors by radiprodil.Brain : a journal of neurology · 2026Article
- Neurodevelopmental disorder-causing GRIN1 Y647S variant alters red blood cell physiology in mice.Physiological reports · 2026Article
- Mice carrying a GluN2B protein-truncating variant have altered NMDA receptor subunit composition and their behavior recapitulates patient phenotypes.Cellular and molecular life sciences : CMLS · 2026Article
- Context-dependent NMDA receptor dysfunction predicts seizure treatment in mice with human GluN1 variant.iScience · 2026Article
- A mouse model of GRIN2D developmental and epileptic encephalopathy recapitulates the human disease.Brain : a journal of neurology · 2026Article
- Synaptic dysregulation in a mouse model of GRIN2D developmental and epileptic encephalopathy.Brain : a journal of neurology · 2025Article
- GRIN2B disease-associated mutations disrupt the function of BK channels and NMDA receptor signaling nanodomains.The Journal of general physiology · 2025Article
- Disruption ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Selective Modulation of the GluN2B/C/D ContainingACS medicinal chemistry letters · 2025Article
- Comprehensive characterization of the RNA editing landscape in the human aging brains with Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Advances in the Structural Basis of GluN2A-Selective Negative Allosteric Modulators.ACS medicinal chemistry letters · 2025Article
- Exploring gene-phenotype relationships in GRIN-related neurodevelopmental disorders.NPJ genomic medicine · 2025Article
- Spermidine Treatment Improves GRIN2B Loss-Of-Function, A Primary Disorder of Glutamatergic Neurotransmission.Journal of inherited metabolic disease · 2025Article
- Ligand distances as key predictors of pathogenicity and function in NMDA receptors.Human molecular genetics · 2025Article
- Identification and validation of integrated stress-response-related genes as biomarkers for age-related macular degeneration.Frontiers in molecular biosciences · 2025Article
- EAR-20 peptide, a novel NMDA receptor positive allosteric modulator.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Considerable genetic variation of N-methyl-d-aspartate receptors (NMDARs) has recently become apparent, with many hundreds of de novo variants identified through widely available clinical genetic testing. Individuals with GRIN variants present with neurological conditions such as epilepsy, autism, intellectual disability (ID), movement disorders, schizophrenia and behavioral disorders. Determination of the functional consequence of genetic variation for NMDARs should lead to precision therapeutics. Furthermore, genetic animal models harboring human variants have the potential to reveal mechanisms that are shared among different neurological conditions, providing strategies that may allow treatment of individuals who are refractory to therapy. Preclinical studies in animal models and small open label trials in humans support this idea. However, additional functional data for variants and animal models corresponding to multiple individuals with the same genotype are needed to validate this approach and to lead to thoughtfully designed, randomized, placebo-controlled clinical trials, which could provide data in order to determine safety and efficacy of potential precision therapeutics.
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