Ask about this productRelated genes to: ADORA1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: ADORA1 Blocking Peptide
- 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 - Ultraviolet-B irradiation (UVB) induces an epidermal damage response including keratinocyte hyperplasia, immune cell infiltration, and the recruitment of follicular melanocyte stem cells to the interfollicular epidermis. Here, we establish the oncofetal chromatin remodeling factor High mobility group AT-hook 2 (Hmga2) as a regulator of these phenotypes through a cyclic-AMP (cAMP) driven process. In this study, we identify somatic tissue expression of Hmga2 in the basal layer of hyperplastic UVB-exposed keratinocytes. Loss of Hmga2 results in the near absence of epidermal hyperplasia, cutaneous neutrophil infiltration, and melanocyte stem cell migration to the interfollicular epidermis. RNAseq of UVB-exposed keratinocytes from wild-type and Hmga2 loss-of-function models reveals increased expression of Adenosine A1 receptor (Adora1), a negative regulator of cAMP. Administration of the cAMP pathway activator forskolin to Hmga2 animals is sufficient to rescue McSC migration, thus highlighting the Hmga2-cAMP axis as a regulator in the cutaneous UVB response. - Source: PubMed
Publication date: 2026/05/25
Donahue Leanne RHsu Chia-HsinYang Youngeun HWong AlexAn LuyeKim DahihmWhite Andrew C - : 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