GRIA2 Antibody
- Known as:
- GRIA2 Antibody
- Catalog number:
- 48-698
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- GRIA2 Antibody
Related 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
- Dysregulation of long non-coding RNA (lncRNA) PART1 is associated with neurodegenerative diseases, but its role in Alzheimer's disease (AD) remains unclear. This study investigated the clinical significance of PART1 in AD and its potential neuroprotective mechanisms, aiming to offer new insights for risk prediction and mechanism research. Serum PART1 levels were detected in 258 participants using real-time quantitative PCR (RT-qPCR), including 70 controls, 88 patients with amnestic mild cognitive impairment (aMCI), and 100 patients with AD. In vitro AD models were established using SH-SY5Y cells treated with amyloid-β peptide 25-35 (Aβ). Functional assays were performed, including flow cytometry and Cell Counting Kit-8 (CCK-8) assay, along with the detection of oxidative stress levels. Mechanism studies included bioinformatic predictions and luciferase reporter assays. Serum PART1 was significantly downregulated in patients with aMCI and AD, and positively correlated with Mini-Mental State Examination scores. Low PART1 expression was a risk factor for AD and demonstrated good diagnostic value (AUC = 0.843). Aβ downregulated PART1 in SH-SY5Y cells, while PART1 overexpression attenuated Aβ-induced cytotoxicity, apoptosis, and oxidative stress. PART1 directly targeted and negatively regulated miR-770-5p, which was upregulated in AD. The neuroprotective effects of PART1 were reversed by miR-770-5p mimic. Furthermore, bioinformatic analysis and validation experiments identified GRIA2 as a downstream target of miR-770-5p. In summary, serum PART1 is a promising biomarker for AD. PART1 exerts neuroprotective effects against Aβ-induced damage by downregulating the miR-770-5p/GRIA2 axis, suggesting that PART1 is a potential target for intervention strategies in AD. - Source: PubMed
Publication date: 2026/09/26
Zhu ShashaLiu MingfangChen JingZhou LiliWang RuimingZhang Guangning - Retinoblastoma (RB) is the most common ocular malignancy in children, but the relationship between environmental pollutants and RB-related molecular alterations remains unclear. This study aimed to identify candidate targets and pathways potentially linking 2.3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with RB. - Source: PubMed
Publication date: 2026/09/09
Wang YingluanHu QiangCao ZhanYe DianSun DaweiQu Lijun - Post-stroke depression (PSD) is a prevalent and debilitating complication of stroke. While ischemic lesion in left prefrontal cortex (PFC) is a recognized risk factor, the underlying mechanisms linking this locus to PSD remain poorly defined. The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit 2 (GluA2) plays a critical role in neuroplasticity and mood regulation. In this study, a PSD rat model was used to investigate the pathophysiological mechanisms in left PFC through behavioral testing, biochemical assays, and pharmacological interventions targeting protein kinase C alpha (PKCα) and protein interacting with C kinase 1 (PICK1)-GluA2 binding. The results demonstrated that PSD reduced membrane GluA2 in left PFC. Mechanistically, PICK1 participated in the phosphorylation of GluA2 by PKCα, which in turn facilitated the reduction of membrane GluA2. Crucially, both inhibition of PKCα and disruption of PICK1-GluA2 binding rescued membrane GluA2 in left PFC without affecting total GluA2 expression and alleviated depressive-like behaviors of PSD rats. These findings suggest that reduced membrane GluA2 in left PFC correlates with PSD and may represent a potentially therapeutic target. - Source: PubMed
Publication date: 2026/09/09
Yu YipengFu RongRong HaokunFang Qi - 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