ADORA3
- Known as:
- ADORA3
- Catalog number:
- 001232A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADORA3
Related genes to: ADORA3
- Gene:
- ADORA3 NIH gene
- Name:
- adenosine A3 receptor
- Previous symbol:
- -
- Synonyms:
- AD026
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-13
- Date modifiied:
- 2019-04-23
Related products to: ADORA3
Related articles to: ADORA3
- Amiodarone (AMD), a highly effective Class III antiarrhythmic drug, has its clinical utility limited by the risk of inducing a serious adverse effect, amiodarone-induced pulmonary fibrosis (AIPF). The pathogenesis of AIPF remains poorly elucidated, particularly the hub driver genes, which hinders early diagnosis and targeted intervention. - Source: PubMed
Publication date: 2026/02/23
Yan XiaoyanLiu YingFan Rui - Sepsis is characterized by profound immunometabolic dysregulation, yet the role of purine precursor synthesis in immune reprogramming remains poorly defined. Intracellular purine nucleotides, such as ATP, are generated by synthesis, which assembles purinosomes to build inosine monophosphate (IMP) from small precursors, or by the salvage pathway, which recycles purine bases such as hypoxanthine. Here, we investigated how these pathways regulate macrophage activation and host responses in sepsis. Silencing the purine enzyme glycinamide ribonucleotide transformylase (GART) in LPS-stimulated macrophages induced marked transcriptomic remodeling, suppressing anti-inflammatory mediators, including IL-10 and TIMP-1, while increasing TNF-α. These effects were reversed by hypoxanthine supplementation, indicating rescue through salvage. Similar findings were observed with silencing of phosphoribosyl pyrophosphate amidotransferase (PPAT) or pharmacological GART inhibition with azaserine or lometrexol, which also reduced intracellular ATP levels in a hypoxanthine-reversible manner. In contrast, inhibition of salvage enzymes (HPRT, APRT) did not alter IL-10 expression. De novo purine synthesis blockade increased Adora2a expression and decreased Adora3 expression without affecting MAPK signaling. Macrophages formed purinosomes under purine-depleted conditions, which disassembled in the presence of exogenous hypoxanthine. In vivo, azaserine treatment in cecal ligation and puncture-induced sepsis reduced IL-10, increased TNF-α, and elevated bacterial burden. LPS-treated macrophages and PBMCs from septic patients showed reduced GART and PPAT expression. These findings identify purine synthesis as a metabolic checkpoint that sustains anti-inflammatory macrophage programming and host defense, highlighting purine metabolism as a potential translational target in sepsis. - Source: PubMed
Publication date: 2026/02/19
Haskó GyörgyLiu LuyuNémeth Zoltán HWagener GebhardAkcan UgurArif MuhammedPacher PálKelestemur Taha - Alternative splicing (AS) is a fundamental mechanism governing transcriptomic diversity and cellular identity. Although 293T (human embryonic kidney) and A549 (human lung adenocarcinoma) cell lines are widely used, cell-type-specific splicing dynamics-including responses to receptor overexpression-remain incompletely characterized. To address this, we integrated Oxford Nanopore long-read sequencing with BGI short-read data to profile transcriptomes under both basal and GPCR-overexpressing conditions (3 in 293T; in A549). Full-length isoform analysis using FLAIR and SQANTI3 revealed extensive transcriptomic complexity, including 18.02% novel isoforms in 293T and 19.52% in A549 cells. We found that 293T cells exhibited a stable transcriptome architecture enriched in splicing-related pathways, whereas A549 cells underwent broader transcriptional remodeling linked to tumorigenic processes. These findings suggest that 293T cells may be a suitable model for investigating splicing regulation, while A549 cells could serve as a relevant system for exploring tumor-related transcriptome dynamics. Our work elucidates context-dependent AS regulation and underscores the value of integrating long-read sequencing with FLAIR/SQANTI3 for dissecting cell-state-specific transcriptome dynamics. - Source: PubMed
Publication date: 2026/01/03
Li XinQue HanyunLiu ZhaoyuXu GuoqingWang YipengCong ZhaotongLeng LiangWu ShaChen Chunyan - High altitude with insufficient oxygen supply poses a great threat to public health. Short- or long-term hypobaric hypoxia (HY) exposure significantly impairs cognitive function. Adenosine receptors with four subtypes participate in the pathogenesis of multiple neurodegenerative diseases. However, the functions of adenosine receptors in HY-induced cognitive impairment are poorly explored. A mouse model of HY-induced cognitive impairment was established using a hypobaric chamber to simulated hypoxia conditions equal to an altitude of 7000 m for 14 days. The levels of adenosine receptors (ADORA1, ADORA2A, ADORA2B and ADORA3) in the hippocampus of cognitively impaired mice was detected by Quantitative Real-time Polymerase Chain Reaction (qPCR) and Western blot. The ADORA2A antagonist KW6002 was administered from day 4 to day 14 of HY exposure. Neurobehavioral function assessments, histopathological staining, evans blue extravasation and transmission electron microscopy were used to evaluate the therapeutic effects of KW6002 in vivo. RNA-seq, qPCR, ELISA, immunofluorescence, and western blots were performed to investigate the underlying mechanism of adenosine A2A receptor in HY-induced cognitive impairment. Adenosine A2A receptor was uniquely upregulated after HY exposure, while the other three subtypes (ADORA1, ADORA2B and ADORA3) were barely influenced. Selective antagonism of ADORA2A by KW6002 strongly attenuated mice neurological deficits and histopathological injuries. Furthermore, KW6002 enhanced the integrity of blood-brain barrier (BBB), mitigated oxidative stress and neuroinflammation. KW6002 potently inhibited the production of endogenous cAMP and cascading mitochondrial protein levels of EPAC1 and VDAC1, which alleviated the release of the mtDNA to cytoplasm via mitochondrial permeability transition pore (MPTP). Less cytosolic mtDNA accumulation after KW6002 treatment attenuated HY-induced activation of cGAS-STING inflammatory signaling pathway. ADORA2A activation mediates HY cognitive impairment, which is achieved by activating EPAC1 and VDAC1 to mediate mtDNA release and cGAS-STING signaling pathway to drive neuroinflammation cascade. - Source: PubMed
Publication date: 2026/01/05
Cheng HongboGao YehuiShang HuiyingHan WeiyeZhang XiaotongGao RongDang WanyunMa ZengchunLiu XianGao Yue - The aim of this study is to elucidate the effects and mechanism of narirutin (NR) in colorectal cancer (CRC). - Source: PubMed
Publication date: 2025/11/14
Wang HaoJiang RongrongLiu CaitangChen Fei