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
- Since the introduction of second-generation antipsychotics, antipsychotics have been increasingly prescribed for children and adolescents, raising concerns about their long-term impact on neurodevelopment. Antipsychotics block dopaminergic and serotonergic receptors, potentially disrupting the maturation of neurocognitive processes, which is a public health concern. Previous studies have reported that adolescent antipsychotic treatment can cause persistent neurocognitive dysfunction in rodents, yet the neurobiological underpinnings remain unknown. To address this, we administered risperidone, a commonly used antipsychotic, to C57BL/6 mice during adolescence (3 to 6 weeks of age) and examined behavioral and neurobiological outcomes nine weeks post-treatment. Risperidone-treated mice exhibited subtle deficits in behavioral correlates of anxiety-like behavior. In vivo, two-photon calcium imaging of cortical neurons revealed a remarkable increase in the amplitude of calcium events with subtle sex-specific changes in the frequency, consistent with increased neuronal excitability. Single-nucleus RNA-sequencing (snRNA-seq) analyses showed widespread reductions in transcripts for voltage-sensitive and inwardly rectifying potassium channels in both pyramidal neurons and interneurons. Additionally, both cell types exhibited reduced Grin2a and Grin2b, as well as scaffolding proteins, indicative of weakened synaptic connectivity between excitatory and inhibitory neurons. Interestingly, we observed sex-dependent differences in the directionality of correlation between certain gene co-expression modules and risperidone treatment. Our results suggest that adolescent risperidone treatment induces lasting transcriptomic and functional changes associated with altered excitatory-inhibitory neuronal interactions that may underline cognitive and behavioral dysregulations. - Source: PubMed
Publication date: 2026/07/08
Alicea-Pauneto Abneil DChoi HyowonZhang WenyuLi XinjianBusque Laurence ALi MingxuanWu AndrewZhang EvanMarc Adam DPreall JonathanWang Kuan HongFeatherstone Robert ESiegel Steven JHahn Chang-GyuBorgmann-Winter Karin E - Cognitive decline is common after cancer, but little is known regarding the etiology of this adverse effect, especially in terms of molecular mechanisms. - Source: PubMed
Publication date: 2026/07/06
Kesler Shelli RFranco-Rocha Oscar YKogon ManuelaBraun SarahTolby LeahNyagaka RuthDe La Torre Schutz AlexaBlayney Douglas WPalesh Oxana - 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