GRIA2 is one of the glutamate receptors, which are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. The
- Known as:
- GRIA2 glutamate receptors, predominant excitatory neurotransmitter receptors mammalian brain activated a variety healthy neurophysiologic processes. The
- Catalog number:
- 31-110
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- GRIA2 one the glutamate receptors which are predominant excitatory neurotransmitter mammalian brain and activated variety normal neurophysiologic processes. The
Related genes to: GRIA2 is one of the glutamate receptors, which are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. The
- 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
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- 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
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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
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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
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