GRIN2A Pre-design Chimera RNAi
- Known as:
- GRIN2A Pre-design Chimera RNAi
- Catalog number:
- H00002903-R01
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- GRIN2A Pre-design Chimera RNAi
Related genes to: GRIN2A Pre-design Chimera RNAi
- 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 Pre-design Chimera RNAi
Related articles to: GRIN2A Pre-design Chimera RNAi
- 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 - Autism spectrum disorder and related neurodevelopmental disorders (NDDs) affect males at two-to-four times the rate of females, yet the environmental contributors to this sex-differentiated vulnerability remain poorly understood. Here, using a clinically translatable postpartum rat model, we show that synthetic oxytocin (OT) administered for postpartum hemorrhage (PPH) prophylaxis ('PPH-OT'), a universally administered obstetric medication, undergoes lactational transfer, confirmed by stable isotope-labeled OT and LC-MS/MS, without altering maternal behavior or neonatal cortical OT receptor expression. In offspring, PPH-OT altered ultrasonic vocalizations during dyadic interaction and caused a male-specific reduction in social approach, without affecting other behavioral domains. Sex-stratified RNA-sequencing of the medial prefrontal cortex (mPFC) revealed pronounced transcriptional dimorphism: males showed 1,732 differentially expressed genes versus 693 in females, and a sex-by-treatment interaction contrast identified 1,229 formally sex-differentiated genes. Male mPFC downregulated genes were significantly enriched for high-confidence NDD risk genes across three independent databases - SFARI score-1 (highest confidence autism genes; OR = 4.56, p = 0.015), DBD autism (OR = 10.34, p = 7.3×10⁻¹²), and SysNDD autosomal dominant (OR = 9.78, p = 8.4×10⁻⁷) - including core regulators of cortical circuit assembly ( , , , , , and ), an enrichment pattern largely restricted to males. Hypothalamic transcriptional changes were pronounced but showed no enrichment for NDD risk genes, establishing mPFC specificity. These findings identify PPH-OT as a candidate environmental modifier of male neurodevelopmental vulnerability and provide a pressing rationale for prospective investigation of neurodevelopmental outcomes in PPH-OT-exposed children. - Source: PubMed
Publication date: 2026/05/21
Serce GokhanGiri TusarSon MinsooWang RenchengLaury MarieGeorge RebeccaMcCullough Katherine BMaloney Susan ETycksen EricGoo Young AhPalanisamy Arvind - 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