NMDAR1 (Phospho-Ser890) Antibody
- Known as:
- NMDAR1 (Phospho-Ser890) Antibody
- Catalog number:
- 11674
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- NMDAR1 (Phospho-Ser890) Antibody
Related genes to: NMDAR1 (Phospho-Ser890) Antibody
- Gene:
- GRIN1 NIH gene
- Name:
- glutamate ionotropic receptor NMDA type subunit 1
- Previous symbol:
- NMDAR1
- Synonyms:
- GluN1
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-18
- Date modifiied:
- 2016-02-05
Related products to: NMDAR1 (Phospho-Ser890) Antibody
Related articles to: NMDAR1 (Phospho-Ser890) Antibody
- Spinocerebellar Ataxia type 2 (SCA2) and Amyotrophic Lateral Sclerosis type 13 (ALS13) are triggered by polyglutamine expansion in Ataxin-2 (ATXN2). To understand these neurodegenerative disorders at the molecular level, the brains of 10-month-old -CAG100-knockin mice were analyzed as microglial, astroglial and neuronal fractions via global RNA sequencing. Data were validated by comparison with the spinal cord oligonucleotide microarray profile or filtered by RNA-seq consistency. Here, we show that the mutation causes a massive inflammatory response in microglia and a reciprocal loss of neuronal transcripts in glial fractions, suggesting severe synapse loss. Beyond these general neurodegenerative signs, we identify pathognomonic changes in the machinery for protein translation and RNA splicing. Glial fractions showed upregulation of (to 2082%), , , , , , , , and as an unspecific neuroinflammatory signature, versus downregulation of axonal (to <19%), and synaptic , , , and mRNAs correlating with circuit disconnection. In all fractions, reductions in , , and were noted versus disease-specific inductions of ribosomal subunits, presumably mirroring the partial loss-of-function of ATXN2 as RNA translation modulator. Selective accumulations of embryonic factors and versus downregulation of adult specify the mutation impact on splicing and translation elongation. As a potential underpinning of toxic gain-of-function, the proteostasis transcript appeared increased in astroglial and microglial fractions. These transcriptome data suggest altered ribosomal and spliceosome machinery, with massive microgliosis versus mild astrogliosis, at the core of SCA2 and ALS13. - Source: PubMed
Publication date: 2026/04/15
Auburger GeorgKandi Arvind ReddyVutukuri RajkumarAlmaguer-Mederos Luis-EnriqueGispert SuzanaSen Nesli-EceKey Jana - Fibromyalgia (FM) is a chronic pain syndrome characterized by central sensitization, in which glutamatergic and purinergic signaling pathways are thought to play critical roles. This study aimed to evaluate the diagnostic potential of serum glutamate ionotropic receptor N-methyl-D-aspartate type subunit 1 (GRIN1), purinergic receptor P2X 1 (P2RX1), and purinergic receptor P2Y 2 (P2RY2) levels in patients with FM. A total of 93 newly diagnosed FM patients and 93 age- and sex-matched healthy controls were included in the study. Serum levels of GRIN1, P2RX1, and P2RY2 were measured using enzyme-linked immunosorbent assay (ELISA). Receiver operating characteristic (ROC) curve analysis was performed to assess the diagnostic performance of these biomarkers. ROC analysis demonstrated good diagnostic accuracy for all three biomarkers. The area under the curve (AUC) values were 0.817 for GRIN1, 0.778 for P2RX1, and 0.842 for P2RY2 ( < 0.001 for all). At optimal cut-off values, GRIN1, P2RX1, and P2RY2 showed sensitivities of 91.4%, 78.5%, and 92.5%, and specificities of 72.00%, 75.3%, and 80.6%, respectively. Serum GRIN1, P2RX1, and P2RY2 levels exhibit strong diagnostic performance in FM and may serve as promising biomarkers reflecting altered glutamatergic and purinergic signaling in disease pathophysiology. - Source: PubMed
Publication date: 2026/03/31
Dogan Sevil CeyhanKaya Gülcihan CinarTuncbilek ZuhalAtas MertTas Ayca - Lidocaine, a widely used local anesthetic, has been reported to exert anti-cancer activity against hepatocellular carcinoma (HCC). However, its molecular mechanisms remain incompletely understood. This study sought to elucidate the mechanisms underlying lidocaine’s effects on HCC. Potential lidocaine targets in HepG2 cells were identified using network pharmacology and transcriptomic profiling. The prognostic and clinical relevance of candidate genes were assessed through bioinformatics analyses. Key targets were validated by RT–qPCR. The functional role of SLC6A3 in regulating HepG2 cell proliferation, apoptosis, migration, and invasion was examined through in vitro assays. Network pharmacology predicted 433 lidocaine targets, while transcriptomic profiling revealed 442 differentially expressed genes. Nine overlapping targets (SLC6A3, CHRNB2, GRIN1, ADRA2C, LIPE, SLC18A2, KCNQ2, TERT, and ALOX12) were enriched in pathways associated with neuronal signaling, synaptic transmission, and drug addiction. Among these, SLC6A3 and TERT were significantly associated with poor prognosis and increased tumor immune infiltration. Both genes demonstrated predictive value for 1- to 2-year survival, with SLC6A3 showing the stronger prognostic relevance. Molecular docking revealed hydrophobic interactions between lidocaine and SLC6A3 (binding energy: −5.6 kcal/mol). Silencing of SLC6A3 markedly promoted apoptosis and suppressed proliferation, migration, and invasion of HepG2 cells. Collectively, these findings suggest that lidocaine inhibits HCC progression by targeting and downregulating SLC6A3. Lidocaine exerts anti-HCC effects by directly targeting and downregulating SLC6A3, thereby inducing apoptosis and suppressing tumor progression. - Source: PubMed
Publication date: 2026/04/07
Li PeiyangTong WulanHe HongLiu HaoYang Xi - Major depressive disorder (MDD) is a common comorbidity of type 2 diabetes (T2D) with low rates of treatment response to antidepressants. The pathophysiology of these conditions overlaps in N-methyl-d-aspartate receptors (NMDARs), which are present in neurons and pancreatic cells. encodes NMDARs and has been associated with depression and T2D; however, its role in the coexistence of MDD and T2D and the treatment response to antidepressants has yet to be explored. - Source: PubMed
Publication date: 2026/02/27
Rodríguez-Ramírez Alejandra MonserratBenitez-Valenzuela MarielaAlcántara-Garcés María TeresaSanabrais-Jiménez Marco AntonioZaragoza-Hoyos Julio UrielDel Valle-Ramírez HumbertoHernandez-Romero VivianaRojas-Martínez AugustoGarcía-Ulloa Ana CristinaCamarena-Medellin Beatriz - N-methyl-D-aspartate receptors (NMDARs) in the prefrontal cortex (PFC) are critical regulators of neuronal excitability, synaptic plasticity, and cognitive function. NMDAR disruptions, including pharmacological blockade and anti-NMDAR encephalitis, can mimic symptoms of schizophrenia. These observations support the glutamate hypothesis of schizophrenia, which posits that symptoms arise from abnormal corticolimbic glutamatergic signaling. Further evidence for this theory includes abnormal expression of NMDARs and decreased dendritic spine density in the PFC of individuals with schizophrenia, as well as altered spine density and synaptic transmission caused by genetic manipulation of NMDARs. However, it is unknown how progressive loss of NMDAR function in the PFC during adolescence-a developmental time period associated with symptom onset in schizophrenia -affects excitatory synaptic structure and function. In this study, we used in vivo genome editing to ablate expression of the Grin1 gene, which encodes the obligate GluN1 subunit of NMDARs, in medial PFC neurons of female and male adolescent mice. We assessed synaptic density and function in layer V pyramidal neurons using whole-cell patch-clamp electrophysiology, integrated with confocal imaging of dendritic spine architecture in recorded neurons. NMDAR ablation caused an early decrease in basilar dendritic spine density, followed by a rebound in spine density and a corresponding increase in AMPAR-mediated synaptic transmission. These effects of pan-neuronal NMDAR ablation were not observed after a more specific manipulation of excitatory neurons. Our findings demonstrate that NMDAR ablation triggers a cascading reorganization of local PFC networks, which may include compensatory processes that maintain allostasis but are impaired in disease states. - Source: PubMed
Publication date: 2026/03/14
Dick Rachel MCunitz Lydia BTorres Pérez AuroraAhmed HabsaAdke Anisha PRivera Quiles CristinaMitchell Jason SMarron Fernandez de Velasco EzequielGrissom Nicola MRothwell Patrick E