Mouse GRIN2A ELISA Kit
- Known as:
- Mouse GRIN2A Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- orb55999
- Product Quantity:
- 96 well
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- Mouse GRIN2A ELISA Kit
Related genes to: Mouse GRIN2A ELISA Kit
- Gene:
- GRIN2A NIH gene
- Name:
- glutamate ionotropic receptor NMDA type subunit 2A
- Previous symbol:
- NMDAR2A
- Synonyms:
- GluN2A
- Chromosome:
- 16p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-18
- Date modifiied:
- 2016-02-05
Related products to: Mouse GRIN2A ELISA Kit
Related articles to: Mouse GRIN2A ELISA Kit
- N-methyl-D-aspartate receptors (NMDARs) play a pivotal role in neurodevelopment. While pathogenic variants in GRIN genes cause a broad spectrum of epileptic and developmental disorders, the precise molecular determinants that drive specific neurodevelopmental courses remain poorly understood. This study aims to utilize high-resolution structural modeling to identify associations between localized conformational alterations in NMDARs and distinct clinical phenotypes. - Source: PubMed
Publication date: 2026/09/01
Wen Si-JiaWang HaoOuyang Shi-JiaZhang Jun-JiaoTan Quan-ZhenLi Shang-RuZhang Yue-HuaWu YeJiang Yu-Wu - Landau-Kleffner syndrome and related epilepsy-aphasia spectrum disorders are characterized by childhood-onset language regression, sleep-activated epileptiform activity, and frequently refractory seizures. This case report describe a boy with normal early development who developed progressive aphasia and non-motor seizures around age three, with electroencephalographic findings consistent with spike-wave activation during slow sleep, while neuroimaging and metabolic evaluations were normal. Standard antiseizure medications and repeated immunotherapy provided no sustained benefit. Genetic testing at age 12 identified a pathogenic heterozygous GRIN2A gain-of-function missense variant (p.T531M), guiding initiation of targeted therapy with memantine, and an NMDA receptor antagonist. Following memantine treatment, the patient showed marked improvement in speech and social interaction together with reduced sleep-related epileptiform discharges, although some deficits persisted. This case underscores the value of early genetic evaluation in refractory epilepsy-aphasia syndromes and supports the potential role of precision NMDA-modulating therapy in GRIN2A-associated epileptic encephalopathy. - Source: PubMed
Publication date: 2026/06/01
Mohammadi MahmoudShervin Badv RezaRezaei ZahraZangooie AlirezaAsgari RezaMashayekhi Narges - Developmental and/or epileptic encephalopathy with spike-wave activation in sleep is a childhood epileptic encephalopathy spectrum where sleep-related spike-wave discharges drive neurocognitive regression during critical developmental periods. This narrative review synthesizes current evidence on underlying mechanisms and presents an updated diagnostic framework. Impaired slow-wave activity downscaling and sleep spindle disruption predict neurocognitive outcomes more robustly than spike-wave index alone, with thalamic integrity emerging as an independent prognostic marker. Genetic diagnoses have been identified in up to 55% of cases, with GRIN2A variants the most common monogenic aetiology. A structured review of published articles detailing 293 individuals confirmed that language, cognitive, and behavioural impairments frequently coincided with, or sometimes occurred independently of, seizure onset. Our proposed diagnostic framework integrates sleep electroencephalogram-prioritizing spindle preservation and slow-wave organization-alongside high-resolution magnetic resonance imaging, trio-based genomic sequencing, and longitudinal neuropsychological assessment. Further research is needed to validate sleep-based biomarkers and determine whether early intervention improves neurodevelopmental outcomes. - Source: PubMed
Publication date: 2026/08/20
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