ADORA2b ELISA kit
- Known as:
- ADORA2b Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADORA2b-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADORA2b ELISA kit
Related genes to: ADORA2b ELISA kit
- Gene:
- ADORA2B NIH gene
- Name:
- adenosine A2b receptor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17p12
- Locus Type:
- gene with protein product
- Date approved:
- 1993-01-19
- Date modifiied:
- 2015-08-24
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- Abnormal expression of adenosine A2B receptor (ADORA2B) may be involved in the development of osteoarthritis (OA). Therefore, it is necessary to explore its role and mechanism in OA progression to understand OA pathogenesis. - Source: PubMed
Li ZhiZhang PengOuyang ChuanweiShen ZhouGuo Genwei - Changes within neurotransmitter systems are associated with variation in anxiety-related behavior. The adenosine signaling pathway has been linked to anxiety, and caffeine has been utilized as a modulator. However, studies have not considered the impact of an individual's stress coping style (e.g., proactive, reactive) and the corresponding differences in neuromolecular signaling that can influence behavioral responses. - Source: PubMed
Klucas Sydney EWong Ryan Y - Esophageal cancer (EC) lacks robust biomarkers to guide prognosis and therapy. Histone chaperone-related genes (HCRGs) shape chromatin states, but their roles in EC remain unclear. We integrated histone chaperone-based transcriptomic stratification with two-sample Mendelian randomization (MR) to identify genes with genetic evidence consistent with EC susceptibility and clinical relevance. - Source: PubMed
Publication date: 2026/04/13
Xia BihanLiu YuzhiZhao RuiDeng Kai - Idiopathic pulmonary fibrosis is a progressive and fatal chronic lung disease with limited treatment options. Its pathogenesis is closely linked to aberrant activation of oxidative stress. The nuclear factor erythroid 2-related factor 2 (Nrf2), a central regulator of antioxidant responses, represents a promising therapeutic target for IPF. Additionally, M2 macrophage polarization and upregulation of the A adenosine receptor (ADORA2B) contribute to fibrosis progression by promoting the secretion of profibrotic mediators such as transforming growth factor-β (TGF-β). Inhalation-mediated drug delivery offers a means to achieve lung-specific targeting, enhancing therapeutic efficacy while reducing systemic side effects. In this study, we developed a biomimetic nanodelivery system (Mul-siRNA@MM) based on M2 macrophage membranes for the codelivery of mulberrin (Mul) and ADORA2B-targeted siRNA. Results indicated that inhalation of Mul-siRNA@MM nanoparticles markedly suppressed reactive oxygen species (ROS) production via activation of the Nrf2 pathway and effectively silenced ADORA2B expression. These actions consequently reduced M2 macrophage infiltration and downstream profibrotic cytokine release, significantly ameliorating bleomycin-induced lung injury and fibrosis in mice. This work not only extends the application of Mul in treating pulmonary fibrosis, but also highlights the potential of inhaled biomimetic nanoparticles as a targeted, safe, and effective strategy for intervening in IPF. It further underscores the therapeutic value of disrupting the crosstalk between oxidative stress and pro-fibrotic signaling pathways. - Source: PubMed
Publication date: 2026/04/16
Li JiachengLi HengbingWang XinyueWang CanSun JiaoQu ChenghaoTian Hui - Metabolic dysregulation within the epithelial immune microenvironment (EIME) drives chronic inflammatory skin diseases like psoriasis, but the immune mechanisms and downstream consequences remain unclear. Here we perform in-depth metabolomic analysis showing that nucleotide metabolism is enhanced in psoriatic patients, with elevated adenosine levels closely correlating with disease severity. Single-cell and spatial transcriptomics analyses revealed that adenosine is primarily generated from a population of CD73 fibroblasts in psoriatic skin through enhanced metabolic processes and catalytic capability. Adenosine acts as a mediator between fibroblasts and keratinocytes, causing mitochondrial dysfunction and generating oxidative stress, resulting in the release of pro-inflammatory mediators in keratinocytes via ADORA2B. Deletion of Cd73 in fibroblasts, Adora2b in keratinocytes, or the use of pharmacological inhibitors of the pathways involved, reduces epidermal inflammation in the imiquimod- and IL-23A-induced mouse skin inflammation models. Our study thus identifies the CD73 fibroblast subsets as regulators of epithelial inflammation through metabolic microenvironment interactions with keratinocytes, providing proof of principle for therapeutic strategies targeting fibroblast-keratinocyte crosstalk in inflammatory skin diseases. - Source: PubMed
Publication date: 2026/04/09
Tian YuziGuo JiaSun JinjianZhang XiaoyeZhou GuoweiYe LinZhang YanLiu PeihuaZhou JunyuXiao ChengengXie XiaoyunXia YangBachelez HervéLiu HongChen Xiang