Ask about this productRelated genes to: NMDAR2B antibody
- Gene:
- GRIN2B NIH gene
- Name:
- glutamate ionotropic receptor NMDA type subunit 2B
- Previous symbol:
- NMDAR2B
- Synonyms:
- GluN2B
- Chromosome:
- 12p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-18
- Date modifiied:
- 2016-02-05
Related products to: NMDAR2B antibody
Related articles to: NMDAR2B antibody
- 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 - As a widely used organic UV filter and emerging environmental pollutant, 4-methylbenzylidene camphor (4-MBC) accumulates in aquatic ecosystems and human tissues, but its developmental neurotoxicity mechanisms remain unclear. This study integrated network toxicology, molecular docking and dynamics simulations, zebrafish experiments, dose-dependent transcriptomics and the adverse outcome pathway (AOP) framework to elucidate the neurotoxic mechanisms of 4-MBC. Network toxicology identified 150 potential targets and 10 core targets (BDNF, DLG4, EGF, etc.), with enrichment analyses highlighting glutamatergic synaptic signaling, MAPK pathway, and DNA replication as candidate key pathways. Molecular docking and dynamics predicted stable binding of 4-MBC to core targets (e.g., DLG4, GRIN2B). Zebrafish exposed to 4-MBC (1, 10, 100 and 1000 μg/L) showed concentration-dependent developmental malformations, lowered hatching rates and suppressed larval locomotion. Transcriptomic analysis identified 311 dose-responsive genes and enriched key pathways, suggesting disrupted glutamatergic transmission, dysregulated MAPK activity and defective DNA replication as potential core drivers. RT-qPCR further verified dose-dependent transcriptional alterations of representative genes at 100 and 1000 μg/L: the synaptic genes bdnf and dlg4 were downregulated, whereas the neurodevelopmental markers ngn1 and shha were upregulated. AOP-based bioinformatic analysis further indicated impaired DNA repair as a potential converged node that may trigger neural progenitor apoptosis and subsequent growth-inhibition phenotypes. Collectively, these findings propose a working model in which 4-MBC disrupts glutamatergic synapses, activates MAPK signaling, and impairs DNA replication to induce developmental neurotoxicity, though direct functional validation of this cascade is warranted, providing insights for environmental and human health risk assessment. - Source: PubMed
Publication date: 2026/09/01
Lu XiaoyangGuan MiaoTang SuqiHu JunxingSun LiWang JingChen JiaoZhang HuijieXu Shixia - Shugan Bushen decoction (SGBS) is widely used for lumbar disc herniation (LDH)-related pain and emotional disturbances, yet its central mechanisms remain unclear. - Source: PubMed
Publication date: 2026/08/30
Huang ZhenyuXu JingyiGao JiahuaLin HangjuanWu QuanChen JiangGao LinchaoPeng XinLou HongkanHu Hongwei - Bisphenols (BPs) are widespread environmental endocrine disruptors, but their potential depression-related neurotoxicity has not been systematically assessed. Here, we combined machine learning (ML), network toxicology, molecular docking, and in vivo experiments to screen 26 bisphenols for depression-related neurotoxic risk. We first integrated bisphenol A (BPA)-related targets with depression-related genes to build a chemical-gene-phenotype-disease network and an adverse outcome pathway (AOP) framework. We then used nine ML algorithms to rank the predicted risk of the 26 bisphenols. Molecular docking showed that the predicted high-risk compounds had strong binding affinity for estrogen receptor 1 (ESR1). The AOP analysis further suggested the involvement of the ESR1-cAMP response element-binding protein 1 (CREB1)-glutamate ionotropic receptor N-methyl-D-aspartate type subunit 2B (GRIN2B) pathway. In vivo experiments showed that BPA exposure caused neuronal damage in the cornu ammonis 3 (CA3) region of the rat hippocampus and significantly reduced the messenger RNA (mRNA) expression of the corresponding genes , , and in hippocampal tissue. Overall, this study screened and prioritized the model-predicted depression-related neurotoxic risk of 26 bisphenols, supports a role for the ESR1-CREB1-GRIN2B pathway in BPA-induced neurotoxicity, and provides mechanistic evidence for bisphenol risk assessment. - Source: PubMed
Publication date: 2026/08/13
Xie LiYuan ShanliangGan LuMa RonghengTang LeiXu QiangLi Weihong - Synaptic dysfunction is a major contributor to cognitive decline in Alzheimer's disease (AD) and represents an attractive therapeutic target. Here, we investigated whether chronic isoserine treatment improves cognition and alters the expression of synaptic-related genes in APP/PS1 mice. Isoserine was well tolerated and did not adversely affect body weight. In the Morris water maze, isoserine improved probe-trial performance in APP/PS1 mice, significantly reducing latency to the first platform-location crossing, while time spent in the target quadrant showed a directionally consistent but non-significant increase. To identify molecular correlates, we profiled 84 synaptic-related genes using a targeted RT Profiler PCR Array. Gene-level factorial analyses identified several nominal treatment-associated effects, but no individual isoserine effect in APP/PS1 mice remained significant after false-discovery-rate correction. In contrast, module-level analyses identified False-discovery rate (FDR)-significant changes in NF-κB/inflammatory, synaptic-maintenance, and glutamatergic-signaling gene-expression modules, with significant genotype × treatment interactions for the NF-κB/inflammatory and synaptic-maintenance modules. Exploratory heatmap and principal component analyses further illustrated disease-context-dependent expression patterns. Western blot analyses showed that isoserine reduced nuclear factor kappa B (NF-κB p65) and NMDA receptor subunit GluN2B (GluN2B) and increased postsynaptic density protein 95 (PSD-95) levels in APP/PS1 mice. These findings suggest that isoserine improves spatial memory retention and coordinately remodels synaptic and inflammatory molecular programs in APP/PS1 mice. - Source: PubMed
Publication date: 2026/08/18
Saitta AlessandraBasilotta RossellaLanza MarikaScuruchi MicheleCasili GiovannaGiovani PietroCopani AgataEsposito EmanuelaOddo SalvatoreCaccamo Antonella