Ask about this productRelated genes to: GRIA2 antibody
- 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 antibody
Related articles to: GRIA2 antibody
- 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 - Friedreich's ataxia (FRDA) is a neurodegenerative disorder caused by frataxin deficiency, characterized by progressive cerebellar dysfunction and neuronal loss. Although synaptic abnormalities are an early feature of FRDA, the molecular mechanisms linking frataxin deficiency to synaptic dysfunction remain incompletely defined. In this study, we investigated post-translational regulation of the AMPA receptor subunit GluR2 in the cerebellum of the frataxin knockdown (FRDAkd) mouse model. GluR2 protein levels are reduced early following frataxin knockdown, despite unchanged mRNA expression and preserved Purkinje cell number. Phosphorylation of GluR2 at regulatory sites (Ser880 and Tyr876) is unchanged relative to total protein, indicating that altered phosphorylation does not account for reduced GluR2 levels. In contrast, acyl-biotin exchange assays and proximity ligation analysis reveal a significant reduction in GluR2 palmitoylation, localized primarily to Purkinje cell somata. This deficit is selective, as palmitoylation of other synaptic proteins is variably affected. Mechanistically, reduced GluR2 palmitoylation associates with decreased expression and palmitoylation of the palmitoyl acyltransferase DHHC3, while levels of depalmitoylating enzymes remain unchanged. In vitro, DHHC3 enhances GluR2 palmitoylation, supporting a direct enzymatic relationship. Partial restoration of frataxin expression rescues GluR2 and DHHC3 protein levels and partially restores GluR2 palmitoylation. These findings identify impaired GluR2 palmitoylation as an early, selective synaptic alteration in FRDA and implicate dysregulated lipid-dependent post-translational modification as a mechanism linking frataxin deficiency to cerebellar synaptic vulnerability. - Source: PubMed
Publication date: 2026/08/09
Mercado-Ayón ElizabethCoulman JenniferLee Jia-YingLancaster EunjooGoga ElliotAsad MohammadWitze EricLynch David R