anti-GRIN2A / NMDAR2A
- Known as:
- (anti-) to-GRIN2A / NMDAR2A
- Catalog number:
- lf-pa43345
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- anti-GRIN2A / NMDAR2A
Related genes to: anti-GRIN2A / NMDAR2A
- 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: anti-GRIN2A / NMDAR2A
Alkaline Phosphatase Conjugated Affinity Purified anti-Swine IgG (H&L) [Goat] Secondary_Antibodies(endo,anti)_((rac,anti)-4-Deschloro-sertraline CAS: Formula: C17H18ClN(Tyr1)-Adipokinetic Hormone I, Rabbit anti-Locusta migratoria(Tyr1)-Adipokinetic Hormone I, Rabbit anti-Locusta migratoria, IF Kit(Tyr1)-Adipokinetic Hormone I, Rabbit anti-Locusta migratoria; IH(Tyr1)-Adipokinetic Hormone I, Rabbit anti-Locusta migratoria; RIA1 JAR WITH WIDE BOTTOM PLATE (ANTI-TILT)1 JAR WITH WIDE BOTTOM PLATE (ANTI-TILT)1-step Polymer HISTO-STAT; HRP anti Hamster (Secondary Reagent Component) for staining Hamster antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Chicken (Secondary Reagent Component) for staining Chicken antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Goat (Secondary Reagent Component) for staining Goat antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Mouse Adsorbed (Secondary Reagent Component) for staining Rat antibody- on- Mouse tissues, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Mouse Secondary Reagent Component) for staining Mouse and Rat antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Rat (SecondaryReagent Component) for staining Rat antibodies, 250 plus slides Related articles to: anti-GRIN2A / NMDAR2A
- Clozapine is the preferred treatment for refractory schizophrenia. However, clozapine use is constrained by the risk of clozapine‑induced seizures (CISs). The molecular mechanisms behind CISs are complex and poorly understood. The objective of this study was to identify the core targets and signaling pathways contributing to CISs using network pharmacology and molecular docking. Potential targets for clozapine and seizures were screened using multiple databases, and overlapping targets were identified. Protein-protein interaction (PPI) networks were constructed using the STRING database and visualized in Cytoscape to identify core targets. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of the core targets were performed, and a disease-target-pathway-drug network was constructed. The docking of clozapine with the core targets was evaluated to determine the stability of their interactions. Of the 656 potential targets for clozapine and 1260 targets for seizure, 104 targets overlapped. PPI analysis of the overlapping targets yielded 12 core targets. KEGG pathway enrichment analysis demonstrated that glutamatergic, dopaminergic, and GABAergic synapses may be key pathways mediating CIS. The molecular docking results showed that clozapine had strong binding affinities for the core targets, BDNF, GRIN2B, GRIN2A, and GAD1. Thus, clozapine may interfere with the glutamatergic, dopaminergic, and GABAergic synaptic pathways by modulating BDNF, GRIN2B, GRIN2A, and GAD1. Modulation of these core targets may contribute to excitatory-inhibitory imbalance in the central nervous system, thereby potentially increasing seizure susceptibility. This study provides an integrative perspective on the potential pathophysiology of CIS and suggests directions for future experimental validation and risk intervention strategies. - Source: PubMed
Publication date: 2026/06/29
Lian DaxiangLi JianHan BoLiu XiaLi RanliMa XiaoyanMao FuqiangZhuo Chuanjun - The genetic basis of extreme cognitive plasticity in human innovators remains poorly characterized. Here, we demonstrate that the genomic architecture underlying scientific innovation significantly overlaps with the polygenic risks for neuropsychiatric phenotypes, such as schizophrenia. Utilizing a comparative genomic approach across psychiatric cohorts (PGC) and the UK Biobank (Scientific Creativity), we identify a coordinated "Vanguard Engine" consisting of hyper-tuned voltage-gated calcium channels ( ), glutamatergic receptors ( ), synaptic plasticity regulators ( ), and the core linguistic-symbolic coordinator ( ). We posit that these variants establish a high-voltage neural environment optimized for associative divergence. Furthermore, we characterize the and loci as critical metabolic governors against thermal overload and identify structural variance in as the epigenetic clamp linking ancestral fuel availability (β-hydroxybutyrate) directly to the transcriptional control of this plasticity network. We conclude that psychiatric pathology is an emergent property of a fuel-mismatch, wherein a high-performance cognitive architecture is sustained by a carbohydrate-heavy diet, leading to systemic thermodynamic failure. This framework provides a unified, mechanistic explanation for the spectrum between extreme cognitive innovation and pathological collapse. - Source: PubMed
Publication date: 2026/06/16
Krantz Bryan A - As the most lethal neuroendocrine tumor, small cell lung cancer (SCLC) can drive its progression by hijacking neuronal mechanisms. At the core of this neural integration is the N-methyl-D-aspartate receptor (NMDAR) complex. However, its pan-cancer expression and clinical significance in SCLC remain poorly understood. We characterized NMDAR transcriptomic profiles across human cancers to develop the NMDAscore, and analyzed three independent European and Asian SCLC cohorts to identify prognostic biomarkers. Furthermore, we investigated the molecular mechanisms of GRIN2A and evaluated the efficacy of GluN2 inhibitors. The developed NMDAscore exhibited significant prognostic correlations in ACC, COAD, KIRC, UVM, KIRP, OV, PCPG, UCS, THCA, THYM, HNSC, KICH, LGG, and PAAD. Focusing on the SCLC cohorts, we identified (encoding the GluN2A subunit) as a statistically relevant prognostic biomarker associated with poor survival. Mechanistically, upregulation correlates with the activation of neuro-synaptic signaling, metabolic reprogramming, genomic instability, and an immune-cold microenvironment characterized by CD8 T cell exclusion. Pharmacological inhibition of GluN2 using dizocilpine and the FDA-approved antagonist memantine suppressed SCLC proliferation and tumorigenicity in vitro, in 3D tumor spheroids and in vivo xenograft models. Collectively, these findings establish as a prognostic biomarker, linking synaptic hijacking, metabolic plasticity, immune evasion, and drug resistance, and identify the therapeutic potentials of the GluN2 inhibitors dizocilpine and memantine for SCLC. - Source: PubMed
Publication date: 2026/05/25
Zhang JiaxunShahatiaili AkezhouliHou YuhanZhou NingHuang KeWang XiaojunWang DongmeiYu ZhentaoFeng XiaoliGao Yibo - Brain dysfunction is a primary symptom of Gulf War illness (GWI). The present study investigated the effects of an amorphous formula of curcumin (CUR) and α-glycosyl isoquercitrin (AGIQ) on neurobehaviors and adult neurogenesis and following synaptic plasticity of produced neurons in the hippocampal dentate gyrus (DG) in a rat GWI model. Ten-week-old rats received GWI-related chemicals and restraint stress for 28 days; thereafter, animals were fed either a diet without supplement or mixed with 0.1% CUR or 0.5% AGIQ for 126 days. GWI treatment adversely affected behavioral endpoints, including novel object recognition, sucrose preference, novelty-suppressed feeding, and contextual fear conditioning. CUR ameliorated all these effects, while AGIQ caused anxiety-like behavior and improved fear extinction learning. GWI treatment downregulated NRF2-KEAP1 pathway-related genes in the DG; both phytochemicals reversed most of these changes. GWI treatment increased CD68 and CD163 microglia populations in the DG hilus; both phytochemicals reversed the increase of CD68 microglia. In the neurogenic niche, GWI treatment decreased GFAP neural stem cells but increased DCX and PCNA cells, decreased hilar SST and GAD67 GABAergic interneurons, and downregulated Pvalb. CUR reversed decreases in GFAP cell and SST interneuron numbers. Both phytochemicals increased VGLUT1 immunoreactivity, restored the VGLUT1/VGAT ratio, and upregulated Bdnf, Gria1, Gria2, Gria3, Slc17a7, Ptgs2, and Mapk1. AGIQ further increased COX2 cell numbers and upregulated Grin2a, Grin2b, and Mapk3. In summary, both phytochemicals may have exerted antioxidant effects and modulated excitatory/inhibitory balance via glutamatergic signaling in GWI animals; CUR was superior to AGIQ at normalizing aberrant neurobehaviors and neurogenesis. - Source: PubMed
Publication date: 2026/06/25
Tang QianShobudani MomokaSakamaki YuriEbizuka YuriZou XinyuKobayashi MioKigata TetsuhitoKoyanagi MihokoNakao TomohiroShibutani Makoto - Gene knockout (KO) techniques are important for understanding gene function and their impact on organismal traits. This study investigates the effects of targeted KO of SCARB1, TYR, and TYRP1 genes in Oujiang Color common carp, focusing on pigmentation changes, metabolic dysregulation, and host-microbiome interactions. Our multi-omics approach revealed that SCARB1 KO led to complete loss of red pigmentation, while TYR and TYRP1 KOs resulted in hypopigmentation and altered pigmentation patterns. Transcriptomic analysis identified seven key genes (PLA2G4, C3, F2, ERN1, UGP2, purA, and GRIN2A), linked to major pathways: glycerophospholipid metabolism, biosynthesis of cofactors, autophagy, and neuroactive ligand-receptor interaction. Notably, we observed significant upregulation of phosphatidylethanolamine (PE) and disruptions in glycolysis and tyrosine metabolism. Histological analysis showed reductions in epithelial and goblet cells, and microbiome profiling indicated shifts in microbial diversity, including significant changes in Firmicutes, Bacteroidetes, and genera such as Pseudomonas, Rhodobacter, Bacillus, and ZOR0006. These findings uncover pigmentation genes as pivotal players in regulating pigmentation, cellular stress, metabolism, and the microbiota. This study improves our understanding of pigmentation regulation in common carp and provides potential molecular targets for color trait improvement in aquaculture species. - Source: PubMed
Kanika Nusrat HasanGuo ZhaoyangMandal Roland NathanHanif Muhammad SajidBao XiaoxiaoChen XiaowenWang JunWang Chenghui