Human Adenosine A2b Receptor,ADORA2b ELISA Kit
- Known as:
- Human Adenosine A2b Receptor,ADORA2b Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- dl-adora2b-hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Wuxi donglin
- Gene target:
- Human Adenosine A2b Receptor ADORA2b ELISA Kit
Related genes to: Human Adenosine A2b Receptor,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
Related products to: Human Adenosine A2b Receptor,ADORA2b ELISA Kit
Related articles to: Human Adenosine A2b Receptor,ADORA2b ELISA Kit
- The Syrian golden hamster () is a universally accepted model for visceral leishmaniasis (VL) due to its ability to mimic human disease pathology. (BALB/c) is preferred for evaluating pharmaceutical and immunological responses. This study focuses on the precise role of gene signatures in -infected and , using transcriptomic analysis. Principal component analysis (PCA) revealed distinct clustering among the four groups (uninfected vs. infected spleen samples from and ). After differential expression analysis, 2054 genes in and 1108 in were found to be differentially expressed, with 153 genes common to both species. Except for 31 genes, most of the commonly dysregulated genes show a similar expression pattern. Although Th1-mediated immune signaling was observed in both cases, the overexpression of in both infected groups underscores the important role of T cell exhaustion. Immunological responses against parasite infection in appear to be more aggressive, while seems more intense. Interestingly, only the -infected group shows overexpression of . Without a definitive role for , the overexpression of , and in both species may drive disease outcome. These findings elucidate the immunological mechanisms driving the pathogenesis of VL in rodent models. - Source: PubMed
Publication date: 2026/06/16
Raj RohitKumari PriyaSen AbhikDikhit Manas Ranjan - Demyelination following subarachnoid hemorrhage (SAH) is an important cause of cognitive impairment in patients. However, its underlying mechanisms remain unclear. This study aimed to elucidate the molecular basis of SAH-related demyelination and identify potential treatments. Contactin-1 (CNTN1) levels in the cerebrospinal fluid were significantly decreased in patients following SAH. Higher levels of CNTN1 expression correlated positively with Montreal Cognitive Assessment (MoCA) scores. However, whether and in which specific cell types CNTN1 expression is downregulated in the SAH brain parenchyma remains unknown. Our single-cell RNA sequencing revealed that Cntn1 was downregulated specifically in neurons, but not in oligodendrocytes. Then knockdown of Cntn1 in neurons via adeno-associated virus (AAV) significantly exacerbated cognitive impairment in mice with SAH. To investigate the mechanisms by which CNTN1 downregulation contributes to cognitive impairment, we performed transcriptome sequencing. This analysis revealed a significant decline in Ada, Plp1, and Mbp following CNTN1 knockdown in neurons. We therefore hypothesized that CNTN1 regulates neuronal ADA and existence of CNTN1-ADA-ADORA2B signaling axis. Through this axis, downregulation of CNTN1 after SAH might lead to demyelination. To validate our hypothesis, we overexpressed Cntn1 in murine neurons using AAV. Results demonstrated that Cntn1 overexpression effectively improved SAH-induced cognitive dysfunction, which can be blocked by ADA enzyme inhibitor. Furthermore, clemastine administration significantly attenuated cognitive impairment following SAH, by mitigating demyelination. Collectively, our results identify neuronal CNTN1 as a critical regulator. Its downregulation exacerbates demyelination through ADA after SAH. Importantly, clemastine might be potential drug used in SAH patients. - Source: PubMed
Publication date: 2026/06/23
Li Long-XiangWei Bo-YangJin LeiWu YuYang Ze-YuLi CanZhou Jia-MingSong YuGong Wen-ZhiOu-Yang Yuan-HaoHuang HaoFeng XinGuo Shen-QuanCheng Wen-PingLi RanLiang Shu-YinSu Shi-XingJin FaZhang XinLiu Yan-ChaoDuan Chuan-ZhiLiu Wen-ChaoLi Xi-Feng - Mild intermittent hypoxia is emerging as a promising strategy to enhance healthspan, but the molecular mechanisms remain poorly defined. ADORA2B, a hypoxia-inducible adenosine receptor, is known to regulate metabolism and stress responses, yet its role in functional aging is unclear. - Source: PubMed
Publication date: 2026/06/19
Capó XavierTorrens-Mas MargalidaCalvo-Navarrete GuillermoGill FrederiqueRaimundo AdelaideSaunter ChristopherCarretero AitorNavas-Enamorado Cayetanode la Llave Ana MolinaSánchez-Polo AndrésMasmiquel LuisWeinkove DavidGonzalez-Freire Marta - Recent studies have emphasized the role of adenosine receptors (ADORs) in the malignant biological behaviors. Therefore, the expression and clinical significance of four subtypes of ADORs (ADORA1, ADORA2A, ADORA2B, and ADORA3) in ovarian tumors were analyzed. - Source: PubMed
Publication date: 2026/06/03
Azizi LeilaBabaei ZeinabKeyvanloo Shahrestanaki MohammadSoltani SetarehPanjehpour MojtabaAghaei Mahmoud - Diethylene glycol dibenzoate (DEGDB), an emerging eco-friendly plasticizer, remains critically understudied with mechanistic and molecular-level evidence linking it to clear cell renal cell carcinoma (ccRCC) progression, representing a major knowledge gap. To fill this gap, we conducted a cross-scale investigation using network toxicology, WGCNA, machine learning, SHAP explainable modeling, and molecular docking as methodological tools to elucidate DEGDB‑induced ccRCC progression. By jointly mining the ChEMBL, PubChem, SwissADME, STRING, and GEO repositories, we rigorously distilled a high-confidence set of 42 target genes, among which TSHR, ADORA2B, ANPEP, CA9, CYP3A4, JUN, NR1I3, and PHGDH were highlighted. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed that DEGDB may propel ccRCC progression by disrupting neuro-endocrine-immune network regulation, activating chemical carcinogenesis-related receptors, and perturbing metabolic-degradation pathways such as nitrogen metabolism and lysosomal signaling. Subsequently, 113 machine-learning algorithms were leveraged to construct predictive models, and SHAP-based interpretation pinpointed five core genes-CA9, NR1I3, PHGDH, GABRA2, and ANPEP. Validation against The Cancer Genome Atlas (TCGA) datasets demonstrated that CA9 exhibits marked expression divergence in ccRCC (box-plot analysis) and is strongly associated with unfavorable prognosis (Kaplan-Meier survival curves). Molecular-docking simulations further confirmed robust binding affinities between DEGDB and all five core target proteins (binding energies < -5 kcal/mol). In vitro assays additionally revealed that DEGDB significantly promotes 786-O and A498 proliferation and up-regulates CA9 protein expression. Collectively, our findings indicate that DEGDB accelerates ccRCC progression via the orchestrated modulation of cellular proliferation, disruption of neuro-endocrine-immune homeostasis, and activation of oncogenic receptors. This study provides a theoretical framework for assessing the environmentally relevant health risks posed by emerging plasticizers and for devising preventive strategies against DEGDB‑induced ccRCC under real‑world exposure scenarios. - Source: PubMed
Publication date: 2026/05/22
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