Human Angiotensin II Receptor 2 ELISA , AGTR2
- Known as:
- Human Angiotensin II Receptor 2 Enzyme-linked immunosorbent assay test , AGTR2
- Catalog number:
- E01A0496
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Angiotensin Receptor 2 ELISA AGTR2
Related genes to: Human Angiotensin II Receptor 2 ELISA , AGTR2
- Gene:
- AGTR2 NIH gene
- Name:
- angiotensin II receptor type 2
- Previous symbol:
- -
- Synonyms:
- AT2, MRX88
- Chromosome:
- Xq23
- Locus Type:
- gene with protein product
- Date approved:
- 1992-08-25
- Date modifiied:
- 2016-10-05
Related products to: Human Angiotensin II Receptor 2 ELISA , AGTR2
Related articles to: Human Angiotensin II Receptor 2 ELISA , AGTR2
- The correlation between renal volume (or mass) and nephron number in newborns allows the use of the total kidney volume (TKV) at birth as a surrogate for congenital nephron number. Previously, the wide variation in final nephron number (termed "nephron endowment") has been attributed to polymorphisms of genes encoding proteins involved in glomerulogenesis, including key genetic variants in the renin-angiotensin system. However, there are no data concerning the role of polymorphism in the gene encoding type-2 angiotensin II receptor () in the modulation of nephron endowment in humans. Therefore, the aim of our study was to analyze the possible association between :rs1403543 polymorphism and kidney volume in Polish full-term healthy newborns. - Source: PubMed
Publication date: 2026/05/05
Miler KarolGorący IwonaŁoniewska BeataLewandowska KlaudynaLica-Miler MartynaRychel MonikaCiechanowicz Andrzej - Dilated cardiomyopathy (DCM) is a clinically heterogeneous cardiac disorder characterized by ventricular dilation and systolic dysfunction, with limited options for mechanism-based diagnosis and targeted therapy. Programmed cell death (PCD), encompassing apoptosis, ferroptosis, pyroptosis, and other regulated mechanisms, has been implicated in the pathogenesis of DCM, yet its diagnostic and therapeutic relevance remains incompletely understood. Here, we performed an integrative multi-omics analysis combining bulk and single-cell RNA sequencing datasets to identify PCD-related molecular features associated with DCM. Through differential gene expression, WGCNA, and six machine learning algorithms, eight core genes (AGTR2, GLI2, HRK, IL10, NQO1, NT5E, SFRP1, and STAT4) were identified and used to construct a predictive model evaluated across five independent cohorts. Immune infiltration and consensus clustering revealed two distinct molecular subtypes with differential immune-metabolic signatures. Single-cell analysis demonstrated cell-type-specific expression, particularly in fibroblasts and immune cells. Drug-gene interaction mapping and molecular docking highlighted decitabine and folic acid as potential therapeutic candidates. Expression of key genes was partially validated at the mRNA and protein levels in both human and mouse myocardium. Notably, given that most transcriptomic datasets represent advanced-stage disease, these findings may reflect shared molecular features of cardiac remodeling rather than early disease-specific mechanisms. This study provides insights into PCD-associated molecular alterations in DCM and offers a basis for future research into molecular stratification and therapeutic targeting. - Source: PubMed
Publication date: 2026/05/18
Fan JiliChen LihongShang WentaoWang XiaotongGan TianTan XinSong LaichunBo Xiaohong - Dextromethorphan (DEX) is a commonly used antitussive agent and N-methyl-D-aspartate (NMDA) receptor antagonist that has been reported to cause different organ impairments. The current investigation was conducted to systematically assess the doses dependent effects of DEX on kidneys. Thirty-two Sprague Dawley rats were categorized into control group, DEX (20 mg/kg), DEX (40 mg/kg) and DEX (80 mg/kg) administered group. DEX exposure led to upregulation of Renin, angiotensin converting enzyme (ACE), and angiotensin II receptor type I (AGTR1) while downregulated the expression of angiotensin II receptor type II (AGTR2), organic anion transporter 1 (Oat1), organic anion transporter 3 (Oat3), organic cation transporter 3 (Oct2), and multidrug resistance-associated protein 2 (Mrp2) in dose-dependent manners. Moreover, DEX intoxication suppressed the activities of catalase (CAT), glutathione peroxidase (GPx), heme-oxygenase-1 (HO-1), superoxide dismutase (SOD), and glutathione reductase (GSR) while promoting the concentrations of reactive oxygen species (ROS) and malondialdehyde (MDA). Similarly, DEX administration caused significant deterioration of renal function as indicated by significant elevations of serum urea, uric acid, blood urea nitrogen, with a marked reduction in the concentration of creatinine clearance. Furthermore, a notable upsurge was observed in the levels of kidney injury molecule-1 (KIM-1), Neutrophilic gelatinase-associated lipocalin (NGAL), N-acetyl glucosamine (NAG), Cystatin-C, Osteopontin, and Endothelin-1 after DEX exposure. Mechanistically, DEX significantly altered the apoptotic balance, elevating the levels of Bcl-2-associated protein X (Bax), cystine aspartic acid protease-3 (caspase-3), and cystine aspartic acid protease-9 (caspase-9) while reducing the levels of B-cell lymphoma-2 (Bcl-2). In parallel, DEX evoked a strong inflammatory response, which was characterized by increased concentrations of nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β) and cyclooxygenase-2 (COX-2). Histopathological evaluation supported these data, as it showed progressive dose-dependent renal damage from tubular degeneration to extensive glomerular collapse, interstitial edema, and inflammation. Collectively, these findings proved that sub-chronic exposure to DEX exerts a marked nephrotoxic effect via coordinated disruption of renal function, inflammatory homeostasis and apoptotic signaling. This study provides new mechanistic insights into DEX-induced renal impairments and emphasizes the importance of a strong regulatory policy. - Source: PubMed
Publication date: 2026/05/01
Alissa MohammedAlghamdi Suad ABinshaya Abdulkarim SAlqarni Adel MSafhi Awaji YSabei Fahad YAlbati Amal AAbalkhail Adil - Nonsynonymous single nucleotide polymorphisms (nsSNPs) in angiotensin Type II receptor () have been identified as a potential cause of cardiovascular illness in humans. Identifying structurally and functionally relevant alterations in is critical to investigate possible therapeutic targets. - Source: PubMed
Publication date: 2026/04/15
Waleed Iqbal MuhammadShahab MuhammadSun XinxiaoAkter ShahinaZheng GuojunShazly Gamal ABourhia MohammedDauelbait MusaabYuan Qipeng - Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in communication, social interaction, and behavioral regulation. Its etiology arises from a combination of genetic vulnerabilities and environmental influences. Bisphenol A (BPA) is an endocrine-disrupting chemical found in plastic-containing materials, including micro- and nanoplastic pollutants. Recent studies have shown that prenatal BPA exposure can alter behavior and the expression of genes related to autism and neurodevelopment. - Source: PubMed
Publication date: 2026/04/17
Sukjamnong SupornSaeliw ThanitPanjabud PawineeThongkorn SurangratKanlayaprasit SongphonLertpeerapan PattanachatHu Valerie WSarachana Tewarit