ADORA3 Pre-design Chimera RNAi
- Known as:
- ADORA3 Pre-design Chimera RNAi
- Catalog number:
- H00000140-R03
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ADORA3 Pre-design Chimera RNAi
Related genes to: ADORA3 Pre-design Chimera RNAi
- 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 Pre-design Chimera RNAi
Related articles to: ADORA3 Pre-design Chimera RNAi
- Adenosine receptors (ADORAs) are G-protein coupled receptors that critically modulate cell function, yet their specific roles in regulating insulin and glucagon secretion remain incompletely understood. While RNA sequencing of isolated human islets, confirmed by qPCR, revealed that only ADORA1 and ADORA2A transcripts are abundantly expressed, mouse islets express all four receptor subtypes (Adora1, Adora2a, Adora2b, and Adora3). Confocal immunofluorescence demonstrated ADORA1 protein localization in both islet β- and α-cells. Transcriptome correlation analysis of human islets identified 87 genes strongly associated with ADORA1 expression, enriched in pathways regulating carbohydrate and lipid metabolism, cell cycle, apoptosis, proliferation, endocrine system development, and metabolic disease. ADORA1 mRNA levels were positively correlated with HbA1c and elevated in islets of type 2 diabetes (T2D) donors, implicating ADORA1 in β-cell dysfunction. In ob/ob mouse islets, reduced Adora1 expression coincided with enhanced pulsatile insulin secretion, while the control islets showed a biphasic with a weaker second phase insulin secretory response. Adenosine efficiently suppressed insulin secretion in both ob/ob and control islets. ADORA1 antagonist DPCPX attenuated adenosine-induced suppression of insulin release. Adora1-KD mice exhibited a restored, pulsatile second-phase insulin response absent in controls. In human islets, adenosine suppressed both glucose-stimulated insulin secretion and cAMP generation, effects prevented by DPCPX. Adenosine also impaired β-cell viability and proliferation, which were rescued by ADORA1 inhibition. Collectively, our findings identify ADORA1 as a key inhibitory modulator of β-cell function under diabetogenic stress, thereby a promising therapeutic target to preserve insulin secretory capacity in early T2D. - Source: PubMed
Publication date: 2026/08/27
Mohammed Al-Amily IsraaParandeh FariborzAmisten StefanDunér PontusMeidute-Abaraviciene SandraGrapengiesser EvaHellman BoSalehi Albert - The ability to tightly regulate and maintain a warm core body temperature (T) is a defining characteristic of homeotherms. Moving to a thermally preferred place is an energetically efficient first-line thermoregulatory mechanism. We optimized a mouse binary thermal preference assay, selecting floor plate temperatures of 38°C versus 25°C for males and 39°C versus 30°C for females as having no baseline preference. Warm preference was increased in females, by fasting, and with age. Genetic manipulations that increased warm preference included ablation of uncoupling protein 1 () or of all four adenosine receptors (, , , ). Ablation of estrogen receptor α () reduced the preference for the warmer side in females but had no effect on preference in males. Mice treated with the β adrenergic receptor agonist CL-316243 or the A3 adenosine receptor agonist MRS5698 sought the cooler surface. Thermal preference assays complement the measurement of T, providing information about whether a change in T reflects a new target or set point T caused by the intervention, or if the mouse is trying to maintain an unchanged T. Thermal preference can be more sensitive than baseline T for detecting changes in thermal physiology. A thermal preference assay optimized for each sex demonstrated preference differences depending on physiologic state, genetic manipulation, and drug treatment. Thermal preference assays provide information that is complementary to measurement of core body temperature. Thermal preference can be more sensitive to perturbations than baseline body temperature and informs the understanding of how genetic, pharmacologic, and physiologic interventions alter thermoregulatory drive. - Source: PubMed
Publication date: 2026/08/06
Xiao CuiyingDemby Tamar CLiu NailiGavrilova OksanaReitman Marc L - Although methotrexate (MTX) is extensively utilized in management of rheumatoid arthritis (RA), its pharmacogenomics are still unclear. This study explores the genetic determinants impacting MTX's effectiveness and adverse effects in Taiwanese patients with RA, aiming to enhance understanding of RA treatment and pharmacogenetics. A retrospective analysis of 1,948 RA patients receiving MTX treatment from January 2009 to January 2022, using data from the Taiwan Precision Medicine Initiative (TPMI) at Taichung Veterans General Hospital. Among these patients, 872 who required treatment with biologic disease modifying anti-rheumatic drugs (bDMARDs) or targeted synthetic DMARDs (tsDMARDs) were classified as MTX 'non-response', while the 1,076 patients treated without these agents were categorized as MTX 'response'. Chi-square analysis was employed to compare the carrier ratio of 82 selected MTX-associated SNPs from previous literature. Logistic regression models were utilized to explore associations between genetic variants and the risk of non-response and adverse effects, with adjustments made for potential confounding factors. Significant genetic markers influencing MTX response included ABCC1 rs212090, which predicted better MTX efficacy (p = 0.016), and ABCC3 rs2277624 and rs4148416, linked to lower MTX response rates (p = 0.004 and p = 0.023). SNPs in ADORA3 rs2298191 and ABCC4 rs7317112 were linked to a higher risk of thrombocytopenia (p = 0.045 and p = 0.049). Our study identifies genetic variations ABCC1 and ABCC3 related to MTX efficacy in treating RA, while SNPs in ADORA3 and ABCC4 are associated with the side effect of thrombocytopenia. These insights offer a foundation for tailoring individual treatment plans based on genetic profiles. - Source: PubMed
Publication date: 2026/06/09
Yu Ta-WeiChen I-ChiehLin Guan-ChengKao Chung-MaoChen Yen-JuChen Yi-Ming - 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 - 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