Human GRIN2A ELISA Kit
- Known as:
- Human GRIN2A Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- abx151742
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Human GRIN2A ELISA Kit
Related genes to: Human 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: Human GRIN2A ELISA Kit
Related articles to: Human GRIN2A ELISA Kit
- Psychiatric disorders are more common in people with epilepsy and vice versa psychiatric patients have an increased risk of epilepsy. Psychosocial factors, medication effects, peri-ictal or interictal symptoms play a role as do shared genetic mechanisms, particularly in rare monogenic epilepsy syndromes. This review article exemplary discusses GRIN2A-associated disorders, development-related and epileptic encephalopathies including Dravet syndrome and tuberous sclerosis complex. Neuropsychiatric manifestations, pathophysiological foundations and targeted treatment are summarized. Emphasis is placed on the systematic assessment of psychiatric symptoms and detailed clinical phenotyping to evaluate disease-modifying effects of emerging therapies beyond seizure control. The article highlights the clinical implications, gaps in care and to present open questions and to promote interdisciplinary neurological psychiatric management. - Source: PubMed
Publication date: 2026/05/29
Baumgartner CarolineBaumgartner TobiasPhilipsen AlexandraSurges RainerSchulte Eva C - Developmental and epileptic encephalopathies (DEEs) with early burst-suppression EEG (EIDEE-BS) are among the most severe neonatal epileptic syndromes, typically presenting in the first months of life with refractory seizures and profound neurodevelopmental impairment. Although variants in the , , and genes are recognized as major causes, the full genetic spectrum remains uncertain. We aimed to delineate the electroclinical characteristics, genetic etiologies, and long-term outcomes in a large MRI-negative EIDEE-BS cohort. - Source: PubMed
Publication date: 2026/05/26
Riccardi FlorenceDesnous BéatriceBorloz EmilieLepine AnneLacoste CarolineMignon-Ravix CécileCacciagli PierreMissirian ChantalMolinari FlorenceMortreux JérémieAfenjar AlexandraAltuzarra CéciliaAuvin StéphaneBar ClaireBarth MagalieBiscaye StéphanieBourel-Ponchel EmilieCabasson SébastienCances ClaudeCastelnau PierreCaubel IsabelleCarneiro MarylineChabrol BrigitteChadie AlexandraChaussenot AnnabelleCheuret EmmanuelChouchane MondherCogné BenjaminColin EstelleDemurger FlorenceDesportes VincentDieux-Coeslier AnneDoummar DianeGoizet CyrilGoldenberg AliceGhoumid JamalGuerrot Anne-MarieHerenger YvanHeron DelphineHorvath GabriellaIlunga SergeIsidor BertrandJeanne MédéricJulia SophieKaminska AnnaLagrue EmmanuelleLambert LaetitiaLebre Anne-SophieLefranc JérémieLesca GaëtanLevrat VirginieMansour HichamMarey IsabelleMarret StéphaneMaurey HélèneMetreau JuliaMignot CyrilNaudion SophieNeveu JulienPatat OlivierPasquier LaurentPerrier Julie BoeswillwaldPetit FlorencePoulat Anne-LiseQuélin ChloéRichelme ChristianRollier PaulRondeau StéphaneRoubertie AgatheSchaefer EliseDe Saint-Martin AnneThauvin ChristelTorre StéphanieToutain AnnickVan Coster RudyVille Dorothée MVilleneuve NathalieVillard LaurentMilh Mathieu - Despite being essential mediators of pain processing, the molecular identity of N-methyl-D-aspartate receptor (NMDAR) subtypes in nociceptive dorsal horn circuits is poorly understood, especially between sexes and in humans. Given the importance of GluN2 subunits in shaping NMDAR function and plasticity, we investigated the expression and localization of specific GluN2 NMDAR variants in the dorsal horn of viable spinal cord tissue from male and female rodents and human organ donors. Analysis of single-cell/nuclei sequencing datasets and quantitative reverse transcriptase polymerase chain reactions (qRT-PCR) revealed that the GluN2A () and GluN2B () subunits are robustly expressed in dorsal horn neurons of mice, rats and humans, with moderate expression of GluN2D (). Immunohistochemistry (IHC) with antigen retrieval demonstrated that GluN2A, GluN2B, and GluN2D proteins are all preferentially localized to the superficial dorsal horn of both adult rats and humans, which is conserved between males and females. Surprisingly, we found that these GluN2 NMDAR subunits are enriched in the lateral superficial dorsal horn in rats but not in humans, while presynaptic and neuronal markers are symmetrically distributed across the rat mediolateral axis. A dramatic shift in localization of GluN2A to the lateral superficial dorsal horn was observed across later postnatal development (PD21-PD90) in both male and female rats, with a corresponding change in synaptic NMDAR currents. This discovery of changes in NMDAR subunit distribution during maturation and between species will shed light on the physiological roles of NMDARs and their potential as therapeutic targets for pain. We used complementary single-cell/nuclei analysis, immunostaining, quantitative reverse transcriptase polymerase chain reactions, RNAscope in situ hybridization, and electrophysiological approaches to compare the relative expression of N-methyl-D-aspartate receptor (NMDAR) GluN2 subunits in dorsal horn spinal cord pain circuits of mouse, rat, and human spinal cord tissue. Through these comparisons, we find that the transcripts and proteins of the GluN2A, GluN2B, and GluN2D NMDAR subunits are robustly expressed in superficial dorsal horn neurons, with conserved expression across sex but important differences in expression and localization patterns across late development and between species. These discoveries shed light on the physiological roles of NMDARs and their utility as potential therapeutic targets for pain. - Source: PubMed
Publication date: 2026/05/21
Griffiths KatherineArmstrong JenniferMartin NewtonMurray-Lawson ClareOneil EstefaniaDavid Laurence STemi SantinaParnell JessicaRudyk ChristopherBursey JuliaKrajewski Jeffrey LMcDermott Jeff SDedek AnnemarieLevine Ariel JLi BaolinTsai Eve CHildebrand Michael E - Neurodegenerative diseases constitute a major public health burden, with neurotoxicity representing a critical pathogenic mechanism underlying Alzheimer's disease and Parkinson's disease. Current therapeutic approaches are primarily symptomatic and fail to prevent disease progression, highlighting the urgent need for neuroprotective agents that can modulate pathological pathways at their source. Natural fungal metabolites have emerged as promising sources of bioactive compounds with potential neuroprotective properties. This study investigates the neuroprotective potential of bioactive compounds derived from the Arctic fungus Pseudogymnoascus australis (P. australis) using an integrated in silico method. From 120 identified compounds, nine were selected based on favorable blood-brain barrier (BBB) permeability and pharmacokinetic profiles using ADMET 3.0 predictions. These included 2-aminohexadecanoic acid (AHA), 11-aminoundecanoic acid (AUA), and seven others, all exhibiting optimal drug-likeness (>0.83) and suitable CNS-targeting properties. Network pharmacology analysis identified 226 overlapping targets between the fungal compounds and neurotoxicity-associated genes. Nine hub genes (Gria1, Gria2, Gria4, Grik1, Grik2, Grin1, Grin2a, Grin2b, and Grin2c) were identified as critical nodes. Enrichment analyses revealed significant involvement in the neuroactive ligand-receptor interaction pathway, suggesting these compounds modulate ionotropic glutamate receptors. Molecular docking analysis showed strong binding affinities, with 78% of ligand-receptor complexes displaying RMSD values below 2.0 Å. AHA and Grik1 emerged as the most promising pair, with a docking score of -7.90 kcal/mol and excellent pharmacokinetic properties (drug-likeness: 0.462, BBB penetration: 0.985). Molecular dynamics simulations over 100 nanoseconds confirmed complex stability, with a mean RMSD of 2.45 Å and binding energies averaging -169.02 kcal/mol, demonstrating sustained ligand-protein interactions. These computational findings provide evidence that P. australis contains bioactive compounds capable of attenuating neurotoxicity through sustained modulation of glutamate receptors, with molecular dynamics validation supporting the thermodynamic stability and potential therapeutic relevance of these interactions. - Source: PubMed
Publication date: 2026/05/17
Naomi RuthAl-Amin MdSmykla JerzyRizman-Idid MohammedChong Teoh TeowMurthy Jaya KumarZubairi Saiful IrwanDavid PamelaSatriawan HerlandBakar Nurlizah AbuAlias Siti Aisyah - Certain events that occur in early life, such as changes in nutrition, can induce structural and functional modifications in brain development, leading to behavioral programing in the offspring. These effects depend on the timing, intensity, and duration of exposure, and may contribute to chronic disorders in adulthood. Artificial non-nutritive sweeteners (NNS), such as saccharin, have recently been proposed as potential developmental disruptors. Saccharin consumption during pregnancy is discouraged, as it can cross the placenta and accumulate in the fetus. - Source: PubMed
Publication date: 2026/04/30
Pacheco-Sánchez BeatrizLópez-Merchán RaquelRubio PabloGarcía-Martos PilarSuárez JuanSanjuan CarlosRubio LeticiaMartín-de-Las-Heras StellaRodríguez de Fonseca FernandoAlén Franciscode Ceglia MarialuisaRivera Patricia