ADORA1
- Known as:
- ADORA1
- Catalog number:
- 001228A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADORA1
Related genes to: ADORA1
- Gene:
- ADORA1 NIH gene
- Name:
- adenosine A1 receptor
- Previous symbol:
- -
- Synonyms:
- RDC7
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-03-11
- Date modifiied:
- 2014-11-19
Related products to: ADORA1
Related articles to: ADORA1
- : Dysregulation of purinergic signaling, particularly CD73 overexpression, influences tumor progression, immune evasion, and chemoresistance in hepatocellular carcinoma (HCC). We aimed to characterize the transcriptional landscape of this system, identify prognostic markers, and investigate how the tumor microenvironment modulates pharmacological response to combined sorafenib and doxazosin in 3D spheroid models. : We integrated RNA-seq data from The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) to identify differentially expressed genes, pathway enrichment, gene co-expression networks, prognostic associations, and machine learning-based biomarker selection. Modulation of key targets was assessed in HepG2 and HepG2/LX-2 spheroids treated with sorafenib and doxazosin using qPCR and flow cytometry. : Transcriptomics revealed dysregulation and network fragmentation. Specifically, analysis of the TCGA cohort indicated that high expression of , , and correlated with poor overall survival. Given the critical role of CD73 in therapy resistance, we evaluated these findings in 3D models. Co-treatment significantly downregulated and mRNA expression, while was specifically reduced in the co-culture setting. For the , effect-size analysis revealed a large magnitude of inhibition in HepG2 spheroids. Although flow cytometry showed that high CD73 protein expression remained stable across treatments in co-culture, the combination therapy overcame stromal protection, significantly increasing apoptosis (active caspase-3) in both mono- and co-culture spheroids compared with vehicle and monotherapy. : We identified a purinergic prognostic signature in HCC and demonstrated that the combination therapy of sorafenib and doxazosin targets the adenosine pathway and specific receptors. We show that the stromal microenvironment sustains CD73 protein expression even under transcriptional inhibition, highlighting the critical role of 3D co-culture models in deciphering therapeutic resistance mechanisms. - Source: PubMed
Publication date: 2026/02/25
de Sousa Arieli CruzWeber Augusto FerreiraKlain ViníciusScholl Juliete NathaliRamos Jéssica Marques ObelarNascimento Natália Baltazar doGiehl Maria LuizaMartins Renata KrugerHeres João VitorDias Camila KehlMarschner RenataFigueiró FabrícioGuma Fátima Costa Rodrigues - Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder shaped by genetic and environmental factors. Phthalates, widely used as plasticizers in consumer products, have gained attention as potential environmental contributors to ASD; however, their pathogenic roles remain insufficiently defined. This study systematically investigated the molecular associations between three common phthalates, diethyl phthalate (DEP), dimethyl phthalate (DMP), and dioctyl phthalate (DOP), and ASD risk using integrated network toxicology and bioinformatics approaches. Intersection analysis of phthalate-associated targets and ASD-related genes revealed shared enrichment in lipid metabolism-related pathways. Protein-protein interaction network analysis identified 10 key targets: FAAH, CYP2C9, CYP24A1, ACHE, CYP11B1, TSPO, PTGS2, MIF, ADORA1, and ALDH3A1. Molecular docking and dynamics simulations indicated stable binding interactions between phthalates and the target. Mendelian randomization analysis further suggested that FAAH and ADORA1 serve as key pathogenic mediators linking phthalate exposure to ASD risk. In vivo experiments demonstrated that C57BL/6 mice exposed to individual or mixed phthalates exhibited ASD-like behaviors, including reduced social interaction, increased repetitive behaviors, and cognitive impairment, with the most pronounced effects observed in the DEP, DMP, and mixed exposure groups. qRT-PCR analysis of hippocampal tissue showed significant downregulation of Faah and upregulation of Adora1 in the DEP group. Collectively, these findings identify FAAH and ADORA1 as central molecular links between phthalate exposure and ASD-related phenotypes from a systems toxicology perspective, providing insight into environmental contributions to neurodevelopment and potential molecular targets for intervention. - Source: PubMed
Publication date: 2026/03/25
Sun YaoLyu LiangZhang XiruiChen ShuangshuangLiu YutongQiao WanyingZhu TikangWang ShutingWang ZuyueZhou DingHai YangFan Lili - All cells secrete extracellular vesicles (EVs) containing nucleic acid cargo, including microRNAs (miRNAs), that regulate the function of receiving cells. G protein-coupled receptors (GPCRs) affect intracellular function via multiple signaling cascades. However, the mechanisms of GPCR intercellular signaling through EV miRNA activity remain unknown. Human U2 osteosarcoma cells expressing native GPCRs were used to selectively stimulate distinct G protein signaling cascades (Gα, Gα, Gα, and β-arrestin) by members of specific receptor subclasses, including the adenosine receptor A1 (ADORA1), the histamine receptor H1 (HRH1), the frizzled class receptor 4 (FZD4), and the atypical chemokine receptor 3 (ACKR3), respectively. We hypothesized that stimulation of specific classes of GPCRs would cause the release of EVs containing miRNAs with receptor-specific up- or downregulated expression, affecting unique pathological downstream signaling cascades. Receptor-specific agonists dose-dependently increased respective signaling cascade intermediates. We found no change in the quantity of EVs (~200 nm diameter), but there were distinct EV miRNA signatures following stimulation of GPCRs. Network analyses of differentially expressed miRNA and their predicted targets validated the linkage between specific receptors and cell function and pathological states. The data can be used to reverse engineer mechanisms involving EV miRNAs for various physiological and pathological processes. GPCRs are major pharmacological targets, so understanding the mechanisms that stimulate or inhibit GPCR-mediated changes in extracellular miRNA signatures could improve long- and short-term therapeutic and unwanted drug effects. - Source: PubMed
Publication date: 2026/03/20
Shi XiaoPalumbo Michelle CBenware SheilaWiedrick JackMarkwardt SheilaJanowsky Aaron J - This study aimed to investigate the potential molecular mechanism of BYHWD in treating epilepsy by regulating the adenosine system, based on network pharmacology, molecular docking, and molecular dynamics simulations. Active components of BYHWD and their targets were screened using databases such as TCMSP and SwissTargetPrediction. Epilepsy-related targets were obtained from GeneCards and OMIM. Compound-target networks and protein–protein interaction (PPI) networks were constructed. GO and KEGG enrichment analyses were performed. Molecular docking and molecular dynamics simulations were employed to validate the binding ability and stability of key components with adenosine receptors (ADORA1, ADORA2A). A total of 33 active components targeting adenosine receptors were screened, among which 13 components could simultaneously act on both ADORA1 and ADORA2A. Enrichment analysis suggested that the mechanism involves neuroactive ligand-receptor interaction, cAMP signaling pathway, and synaptic function regulation. Molecular docking showed that multiple components had high affinity for the receptors. Molecular dynamics simulations further confirmed the stable binding of isorhamnetin with ADORA2A, with a binding free energy of −26.51 kcal/mol. BYHWD exerts anti-epileptic effects by synergistically regulating adenosine receptors (ADORA1, ADORA2A) and their downstream signaling pathways through multiple active components, thereby restoring the excitatory/inhibitory balance of the neural network. - Source: PubMed
Publication date: 2026/03/08
Wu SitongDeng YuhanYang JiayuePeng ZhuolingChen Jiatong - Epilepsy is clinically heterogeneous and frequently drug-resistant, motivating genetics-informed target prioritization with clinical tractability. Two-sample Mendelian randomization using whole-blood cis-eQTL instruments estimated associations between genetically proxied gene expression and the odds of epilepsy in FinnGen R11 (14,089 cases). For MR-prioritized genes, Bayesian colocalization assessed whether eQTL and GWAS signals were statistically consistent with a shared causal variant at each locus. Biological plausibility and potential safety liabilities were contextualized via protein-protein interaction analysis, functional enrichment, and phenome-wide association screening. ADORA1 and TKT met the prespecified Tier 1 colocalization criterion (PPH4 ≥ 0.90), indicating high posterior probability consistent with a shared causal variant at their respective loci. EP300, CXCR6, and CLEC3B showed suggestive colocalization (0.80 ≤ PPH4 < 0.90) and were retained as secondary, hypothesis-generating signals. Functionally, prioritized genes map to pathways related to adenosine signaling, epigenetic regulation, immune-vascular biology, and metabolism. For pharmacological contextualization, compound-gene signature resources were queried, with triage excluding agents with established severe toxicity, carcinogenicity, or environmental pollutant status and annotation of remaining hits by regulatory status. Molecular docking was used as a structural plausibility screen; docking scores were not interpreted as evidence of in vivo efficacy, safety, or clinical druggability. Inference is constrained by blood-derived regulatory instruments and outcome evidence from a single GWAS cohort; brain-relevant regulation and generalizability require replication. This study provides a transparent genetics-informed framework and a tiered candidate set for discovery-stage mechanistic validation in epilepsy. - Source: PubMed
Publication date: 2026/02/14
Li DongMa YazhouChen XinZhou FeifanXu YuhuaLian Xuegan