GRIN2A Antibody (Center) Blocking Peptides
- Known as:
- GRIN2A Antibody (Center) Blocking Peptides
- Catalog number:
- BP11331c
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- GRIN2A Antibody (Center) Blocking Peptides
Related genes to: GRIN2A Antibody (Center) Blocking Peptides
- 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: GRIN2A Antibody (Center) Blocking Peptides
Related articles to: GRIN2A Antibody (Center) Blocking Peptides
- 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
Rasheed AyshaSekar ShivaniNaqvi RameezDutta ManidipaIssa ManalMenounou AngelikiKrishnakumar DeepaRatnaike Thiloka - Rhodiola crenulata (Hook. f. et Thoms.) H. Ohba is a traditional Tibetan medicine that has long been used in China for its cardioprotective, Qi-tonifying, and mind-calming properties. It is traditionally indicated for conditions such as irritability, restlessness, and agitation. Among its major active constituents are two naturally occurring small-molecule phenols-salidroside (SAL) and its aglycone tyrosol (TYR). While SAL has been reported to exert neuropsychiatric effects including anxiolytic activity, the underlying mechanisms remain incompletely understood, and whether TYR shares similar anxiolytic properties has yet to be clarified. - Source: PubMed
Publication date: 2026/08/19
Cui JunboJia ChunxueWang ZixinSun YuhanLiang YuluLiu ChuanxinHuang Jianmei - Gastric cancer remains a major cause of cancer-related mortality worldwide, highlighting the need for an improved understanding of its molecular mechanisms. Purinergic and glutamatergic signaling pathways, immune checkpoint molecules, and oxidative stress are thought to contribute to tumor biology; however, their combined evaluation in gastric cancer is limited. - Source: PubMed
Publication date: 2026/07/09
Coskun HakkiTuncbilek ZuhalGenc Husnu CagriKaya Gulcihan CinarTas Ayca - Febrile seizures (FS), the most common early-childhood neurological emergency, have a poorly understood impact on the maturing glutamatergic system. We present a detailed spatiotemporal analysis of transcriptional dynamics of key glutamatergic components during a critical postnatal window. Using a hyperthermia-induced FS model in rats at postnatal day 10, we measured mRNA levels of ionotropic (NMDA, AMPA) subunits, metabotropic glutamate receptor (mGluR) groups I-III, glutamate transporters (Slc1a1-3), and glutamine synthetase (Glul) across the dorsal/ventral hippocampus, temporal and medial prefrontal cortices at P14, P21, and P50. For selected targets (GluN2A/2B, GluA1/2, EAAT2), protein abundance was analyzed by Western blotting to test how closely transcriptional changes are reflected at the protein level. We identified robust region- and age-specific developmental trajectories for all targets, including the expected maturational shift in NMDA receptor subunits. FS disrupted these programs, causing widespread downregulation of NMDA and AMPA receptor subunits, mGluRs, and astrocytic transporters in the dorsal hippocampus and temporal cortex at P14. Importantly, FS prevented the normal developmental increase in the Grin2a/Grin2b mRNA ratio in the dorsal hippocampus at P21. Notably, protein abundance for selected targets did not mirror transcriptional changes at the examined time points, suggesting post-transcriptional buffering or delayed translation. This mismatch suggests that transcriptional changes may precede detectable proteomic alterations during circuit maturation, although alternative explanations, such as delayed translation or post-translational regulation, cannot be excluded. Our findings identify candidate transcriptional correlates that may contribute to long-term neurocognitive vulnerability, and highlight the potential importance of timing when targeting glutamatergic pathways for neuroprotection. - Source: PubMed
Publication date: 2026/07/25
Kovalenko Anna AZakharova Maria VSchwarz Alexander PZubareva Olga EZaitsev Aleksey V