Gria2 siRNA_Lentivectors
- Known as:
- Gria2 siRNA_Lentivectors
- Catalog number:
- i064710c
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Gria2 siRNA_Lentivectors
Related genes to: Gria2 siRNA_Lentivectors
- Gene:
- GRIA2 NIH gene
- Name:
- glutamate ionotropic receptor AMPA type subunit 2
- Previous symbol:
- GLUR2
- Synonyms:
- GluA2, GLURB
- Chromosome:
- 4q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-26
- Date modifiied:
- 2016-02-05
Related products to: Gria2 siRNA_Lentivectors
Related articles to: Gria2 siRNA_Lentivectors
- This study aimed to explore the protective effect of Agaricus bisporus polysaccharide (ABP) against high-fat diet (HFD) induced cognitive impairment (CI), with a particular focus on gut-brain communication. ABP supplementation alleviated anxiety-like behavior and cognitive deficits in HFD-fed mice. These effects were associated with enhanced hippocampal synaptic plasticity and attenuated inflammatory responses, which were accompanied by the elevation of Bdnf levels and the upregulated expression of plasticity-related genes (e.g., Gria2, Grin2b, Tdp2, and Fxr1). Crucially, ABP supplementation was associated with alleviated HFD-induced morphological changes in microglia and reduced inflammatory factor mRNA levels (Tnf, Il1b). Meanwhile, ABP remodeled the gut microbiome, significantly enriching beneficial taxa including Akkermansia and Bacteroides and enhancing the production of short-chain fatty acids (SCFAs), mainly acetate and propionate. These findings suggest that ABP may serve as a promising nutritional component for alleviating diet-related CI with effect associated with modulation of the microbiota-gut-brain axis. - Source: PubMed
Publication date: 2026/08/07
Fu ChujingYe KaiQiu ZhichangHu XinyuWang XiaoxuanXiao Hang - Aggressive behavior is a critical issue affecting health and survival in aquaculture animals; however, the molecular mechanism of aggression in reptiles has not been fully understood. Using the Chinese softshell turtle (Pelodiscus sinensis) as a model, we established a turtle model of reactive aggression using the intruder experiment to compare aggressive and non-aggressive individuals. Integrated brain transcriptomic and metabolomic analysis revealed enrichment in glutamatergic and GABAergic pathways between aggressive and non-aggressive individuals. Aggressive individuals showed upregulated glutamate receptor genes (GRIA2, GRIA3, GRIK3) and an altered GABAergic system. Correlation networks confirmed coordinated gene-metabolite covariation in these pathways. Drug injection tests demonstrated that NMDA receptor antagonist MK-801 significantly reduced attacks, indicating that glutamatergic signaling is a primary driver of aggressive behavior. These findings highlight conserved excitatory mechanisms in vertebrate aggression with reptile-specific characteristics and offer targets for low aggressiveness breeding in aquaculture. - Source: PubMed
Publication date: 2026/08/19
Mo JialeZhao EnhaoWang ZongjiGe ChutianYang Han - Glutamatergic neuron-to-glioma signaling mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) has emerged as an important mechanism in glioma progression. We analyzed the expression of the AMPAR subunit genes , , , and in lower-grade glioma (LGG). Expression of - was highest in IDH-mutant/1p19q-codeleted tumors and lowest in IDH-wildtype tumors across both The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA) cohorts. High expression of each gene was associated with longer overall survival (OS). Transcriptome-wide analyses identified positive correlations between an AMPAR score and genes involved in synaptic organization, neuronal connectivity, and neurotransmission. Co-expression analyses demonstrated coordinated expression between - and genes encoding AMPAR auxiliary proteins. Gene Ontology (GO) enrichment revealed overrepresentation of synaptic signaling, trans-synaptic communication, and synapse organization. Although the AMPAR score was associated with favorable survival in univariate analyses, it did not retain independent prognostic significance after adjustment for key clinicomolecular variables. Elevated expression of AMPAR subunit genes in LGG was associated with favorable molecular subtypes and a synaptic transcriptional program. These findings suggest that - expression is associated with a synaptically enriched transcriptional program in LGG, although its cellular origin remains uncertain. - Source: PubMed
Publication date: 2026/07/23
Rodrigues BrunoDalmolin MatheusDal-Pizzol Henrique RitterMalafaia OsvaldoFernandes Marcelo A CCoelho Karina Munhoz de Paula AlvesRoesler RafaelIsolan Gustavo R - The adenosine deaminases acting on RNA (ADAR) family of enzymes (ADAR1 and ADAR2) catalyze adenosine-to-inosine (A-to-I) RNA editing. This post-transcriptional change is remarkably prevalent in the central nervous system (CNS). ADAR-mediated editing is critical for proper brain development, synaptic plasticity, and immunological homeostasis in the central nervous system (CNS) via recoding neurotransmitter receptors and ion channels. Conversely, a wide range of CNS disorders, such as neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis), neuropsychiatric conditions (schizophrenia, bipolar disorder, and major depression), cerebrovascular diseases, and gliomas, are now linked to dysregulation of ADAR activity, whether through loss-of-function mutations, altered expression, or mislocalization. To address the main question of whether altered RNA editing is a fundamental driver of pathogenesis, a compensatory response, or a context-dependent modulator, this review critically synthesizes existing evidence. The basic processes of ADAR enzymes and their regulation throughout neurodevelopment are first described. Next, we thoroughly assess the unique molecular fingerprints of ADAR dysregulation across several CNS disorders, emphasizing recurring themes such as Alu RNA hypo-editing, induction of innate immunity, and GRIA2 editing, which can cause excitotoxicity. Lastly, we examine new treatment approaches that use or reinstate ADAR activity, such as small-molecule modulators and site-directed RNA editing tools (leveraging endogenous ADAR for programmable editing of RNA [LEAPER], clustered ADAR-recruiting guide RNAs (gRNAs) for effective RNA editing [CLUSTER], and mimicking inverted repeats to recruit ADARs using engineered oligoribonucleotides [MIRROR]). We summarize by reviewing key obstacles to clinical translation, including crossing the blood-brain barrier, the risks of off-target editing, and the challenges of achieving spatiotemporal accuracy. We also list important open topics for further investigation. - Source: PubMed
Publication date: 2026/07/25
Zheng FushuangGuan RongliYu XiaojinYang JiaxinZhao HaiYang Fan - The preBötzinger complex (preBötC) is a medullary network that generates the inspiratory phase of respiratory rhythm in mammals and depends critically on glutamatergic transmission. To characterize the anatomical organization of excitatory signaling elements within this network, we analyzed the distribution, morphology, and colocalization of the AMPA receptor subunit GluA2 and the NMDA receptor subunit NR1, together with the postsynaptic scaffold protein PSD95. We also used immunofluorescence and confocal microscopy to examine the spatial relationship between GluA2-positive puncta and the astrocytic glutamate transporter EAAT2 in the preBötC of adult male rats. NR1-positive puncta were more abundant and densely distributed than GluA2-positive puncta, whereas GluA2-NR1 colocalized puncta constituted only a small fraction of either receptor population. NR1-positive puncta also showed limited colocalization with PSD95-positive puncta, indicating that a substantial fraction of NR1 immunoreactivity is not associated with PSD95-defined postsynaptic domains under the present imaging conditions. In contrast, GluA2-positive puncta displayed a non-random spatial proximity with EAAT2 astrocytic profiles and were frequently located within submicron distances. Together, these findings reveal a spatially differentiated organization of glutamatergic elements in the preBötC, characterized by abundant non-PSD95-associated NR1-positive puncta and close apposition between GluA2-positive puncta and EAAT2-immunoreactive astrocytic profiles. This organization provides an anatomical framework for future studies testing how glutamate receptor localization and glutamate clearance mechanisms contribute to excitability and respiratory rhythm generation and modulation. - Source: PubMed
Publication date: 2026/08/06
Olmos-Pastoresa Carol AlejandraVázquez-Mendoza EnriqueVázquez-Martínez OliviaLópez-Meraz María LeonorBeltran-Parrazal LuisMorgado-Valle Consuelo