ADORA2a ELISA kit
- Known as:
- ADORA2a Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADORA2a-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADORA2a ELISA kit
Related genes to: ADORA2a ELISA kit
- Gene:
- ADORA2A NIH gene
- Name:
- adenosine A2a receptor
- Previous symbol:
- ADORA2
- Synonyms:
- RDC8
- Chromosome:
- 22q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1991-03-11
- Date modifiied:
- 2014-11-19
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- The chemical constituents and neuroprotective potential of remain insufficiently characterized. Therefore, we isolated and identified five secondary metabolites (-) from , and investigated their neuroprotective activities and underlying mechanisms. Compound showed the most significant protective effect against HO-induced cytotoxicity in C17.2 neural stem cells. Spectroscopy was used to structurally characterize the isolated compounds. Using RNA sequencing (RNA-seq), compound was found to significantly modulate genes associated with G protein-coupled receptor (GPCR)-related signaling pathways and neuroactive ligand-receptor interactions. Differentially expressed genes, including , , , , and , were validated using quantitative real-time PCR. They are associated with GPCR-related signaling and neurotransmission pathways, consistent with the RNA-seq data. As indicated by the functional enrichment analysis, compound may regulate neuronal stress responses through GPCR-associated signaling networks. In the Western blot, compound markedly attenuated HO-induced protein kinase A (PKA) C phosphorylation without altering total PKA C expression, suggesting that modulation of the cAMP/PKA signaling pathway may contribute to the neuroprotective effects of compound . Collectively, compound may exert neuroprotective effects against oxidative stress-induced neuronal injury, potentially through the modulation of GPCR-mediated PKA signaling. is a promising natural bioactive compound source for further development in neuroprotective research. - Source: PubMed
Publication date: 2026/09/07
Li LuZou GuoweiWang QiaonaJiang HaitaoWu XianghuaZhao JunliZhang HonglinWang XiaopingLi Shengjie - The normalization of ethanol consumption in Western societies represents a major public health concern, particularly when drinking begins during adolescence. The ketogenic diet (KD) has demonstrated therapeutic potential in various conditions, including substance use disorders. This, together with evidence showing that the diet does not significantly affect locomotor activity or aversive and spatial memory in adolescent male mice, makes it an interesting tool for addressing ethanol consumption during a critical developmental period: the transition from adolescence to young adulthood. However, the lack of evidence in females highlights an important gap in current research. This study aimed to evaluate the effects of a KD during adolescence on behavioral profile and ethanol consumption during young adulthood in female OF1 mice. In Experiment 1, behavioral profile was assessed after administration of a KD or control diet from postnatal day (PND) 25 to PND 48. Motor activity, anxiety-like behavior, memory, and learning were evaluated. In Experiment 2, ethanol consumption was assessed using the Drinking in the Dark and operant self-administration paradigms following dietary intervention from PND 39 to PND 82. The KD did not alter locomotion, anxiety-like behavior, or aversive memory, but enhanced hippocampus-dependent spatial memory. Molecular analyses revealed changes in gene expression, including Adora2a, Opmr1, Drd1, Cnr1, and Il-6. Additionally, KD significantly reduced ethanol consumption, which was associated with altered expression of Crhr1, Drd2, Adora2a, and Adora1. These findings support the potential of KD as a therapeutic strategy for reducing ethanol intake in females without negatively impacting behavioral development during adolescence. - Source: PubMed
Publication date: 2026/09/05
Torres-Rubio LauraMellado SusanaMontagud-Romero SandraPascual MaríaRodríguez-Arias Marta - Repeated morphine administration for managing persistent pain frequently induces both physical and psychological dependence, accompanied by alterations in cortical gene expression. To elucidate the molecular underpinnings of morphine dependence, gene expression in the frontal cortex of mice subjected to acute and chronic morphine treatment was profiled using microarray analysis and validated by semi-quantitative PCR. Genes including and were upregulated following both acute and chronic morphine treatment. Gene ontology analysis revealed significant enrichment of differentially expressed genes in membrane components, GPCR signaling pathways, and neurological system processes, indicating integrated alterations in receptor-mediated signaling and downstream transcriptional regulation. Consistent with this, selective phosphorylation of CREB was observed during naloxone-precipitated withdrawal, highlighting CREB-dependent transcription as a key molecular correlate of cortical neuroadaptation. Behavioral assays confirmed robust physical and psychological dependence, supporting the functional relevance of these molecular changes. Collectively, these findings identify a GPCR-centered molecular framework in which coordinated regulation and functional interaction of receptors such as DRD2 and ADORA2A, along with associated signaling components, contribute to morphine-induced neuroplasticity and dependence. These insights may provide a foundation for the development of targeted therapeutic strategies to mitigate opioid dependence. - Source: PubMed
Publication date: 2026/08/31
Kim MijinMoon SohyeonYayeh TaddesseVilla TheaOh Seikwan - Pleasant aroma is a defining sensory trait of Purple-Leaf White Tea (PWT), strongly influencing consumer preference, yet its key chemical contributors remain poorly understood. Using GC-MS combined with comprehensive sensory evaluation, six key aroma compounds-cedrol, β-ionone, geranylacetone, α-terpineol, β-cyclocitral, and (-)-terpinen-4-ol-were identified as major contributors to perceived pleasantness. Sensory analysis revealed significant differences among individual compounds, while their mixture exhibited enhanced pleasantness compared with single compounds. Molecular docking predicted that individual compounds bind to ADORA2A (-6.5 to -5.2 kcal/mol), mainly via hydrophobic interactions. The six-compound mixture showed a markedly lower predicted binding energy (-21.86 kcal/mol). Omission tests indicated that cedrol and α-terpineol contributed substantially to mixture pleasantness, whereas geranylacetone was associated with reduced pleasantness. These findings provide computational support for potential interactions between key aroma compounds and ADORA2A and offer a hypothesis-generating framework for understanding aroma-associated pleasantness in PWT. - Source: PubMed
Publication date: 2026/08/29
Gao ChenxiWu WeiweiZheng ZhiqiangWang ZhihuiYang YaoHe BiyunHuang YanCao ShixianYu ShuntianChen ZhidanSun Weijiang - Adenosine receptors (ADORAs) are G-protein coupled receptors that critically modulate cell function, yet their specific roles in regulating insulin and glucagon secretion remain incompletely understood. While RNA sequencing of isolated human islets, confirmed by qPCR, revealed that only ADORA1 and ADORA2A transcripts are abundantly expressed, mouse islets express all four receptor subtypes (Adora1, Adora2a, Adora2b, and Adora3). Confocal immunofluorescence demonstrated ADORA1 protein localization in both islet β- and α-cells. Transcriptome correlation analysis of human islets identified 87 genes strongly associated with ADORA1 expression, enriched in pathways regulating carbohydrate and lipid metabolism, cell cycle, apoptosis, proliferation, endocrine system development, and metabolic disease. ADORA1 mRNA levels were positively correlated with HbA1c and elevated in islets of type 2 diabetes (T2D) donors, implicating ADORA1 in β-cell dysfunction. In ob/ob mouse islets, reduced Adora1 expression coincided with enhanced pulsatile insulin secretion, while the control islets showed a biphasic with a weaker second phase insulin secretory response. Adenosine efficiently suppressed insulin secretion in both ob/ob and control islets. ADORA1 antagonist DPCPX attenuated adenosine-induced suppression of insulin release. Adora1-KD mice exhibited a restored, pulsatile second-phase insulin response absent in controls. In human islets, adenosine suppressed both glucose-stimulated insulin secretion and cAMP generation, effects prevented by DPCPX. Adenosine also impaired β-cell viability and proliferation, which were rescued by ADORA1 inhibition. Collectively, our findings identify ADORA1 as a key inhibitory modulator of β-cell function under diabetogenic stress, thereby a promising therapeutic target to preserve insulin secretory capacity in early T2D. - Source: PubMed
Publication date: 2026/08/27
Mohammed Al-Amily IsraaParandeh FariborzAmisten StefanDunér PontusMeidute-Abaraviciene SandraGrapengiesser EvaHellman BoSalehi Albert