GRIA2 ELISA kit
- Known as:
- GRIA2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-GRIA2-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- GRIA2 ELISA kit
Related genes to: GRIA2 ELISA kit
- 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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- 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 - Postoperative cognitive dysfunction (POCD) is a common complication of surgery in elderly patients and is characterized primarily by memory impairment; however, the underlying mechanisms remain incompletely understood. By utilizing a laparotomy model in aged mice and the delayed spatial alternation task (DSAT), we found that surgery specifically impaired the memory consolidation process. Importantly, this impairment was accompanied by significant disruption of sharp-wave ripples (SPW-R) in the hippocampal CA1 region. Previous research has indicated that trafficking of GluA2-containing AMPARs at CA3 recurrent synapses is crucial for SPW-R generation. Therefore, we examined postsynaptic AMPARs in the CA3 region after surgery and observed reduced membrane expression of GluA2-containing AMPARs, although the total protein levels and gene transcription remained unchanged. Immunofluorescence and coimmunoprecipitation revealed significantly decreased colocalization and binding of GluA2 with postsynaptic density protein 95 (PSD95), suggesting impaired synaptic GluA2 trafficking. Importantly, immediate postoperative injection of TAT-GluA2 into the CA3 region to increase GluA2 synaptic expression significantly ameliorated surgery-induced SPW-R disruption and memory consolidation deficits. Conversely, local injection of a GluA2 cross-linking agent into the CA3 region of aged mice to inhibit GluA2 trafficking mimicked the postoperative phenotypes of SPW-R disruption and memory consolidation deficits. These results reveal that surgical trauma induces impaired GluA2 trafficking at hippocampal CA3, leading to CA1 SPW-R disruption and ultimately resulting in memory consolidation deficits. This discovery provides not only a novel molecular and neural circuit explanation for the pathogenesis of POCD but also an experimental foundation for the development of neuroprotective strategies targeting GluA2 trafficking. - Source: PubMed
Publication date: 2026/07/06
Xu Zi-QingLi Xiao-WeiWang Gui-ChengWang XuWu Jiang-NanWu Ming-YuWu Ming-HuiWang Gong-MingZhang Meng-Yuan - Early-life environment may influence long-term neurodevelopment through epigenetic regulation. Serotonergic and glutamatergic pathways are central to brain development and have been implicated in DNA methylation changes following prenatal adversity. In this study, we examined whether preterm birth (PTB) in birthweight-discordant twins is associated with differential DNA methylation in the serotonin receptor signaling pathway and the glutamatergic synapse pathway in adult twins. - Source: PubMed
Publication date: 2026/06/10
Rasmussen Carl Peter VittrupNygaard MarianneNielsen Morten FrostSoerensen MetteChristensen KaareTan Qihua - 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