ARNT Antibody
- Known as:
- ARNT Antibody
- Catalog number:
- 32101
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- ARNT Antibody
Related genes to: ARNT Antibody
- Gene:
- ARNT NIH gene
- Name:
- aryl hydrocarbon receptor nuclear translocator
- Previous symbol:
- -
- Synonyms:
- HIF-1beta, bHLHe2
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-01-22
- Date modifiied:
- 2016-10-05
Related products to: ARNT Antibody
Related articles to: ARNT Antibody
- Pseudomonas aeruginosa frequently infects chronically diseased lungs and exacerbates airway mucus hypersecretion and failure in clearance. P. aeruginosa is metabolically versatile and secretes multiple volatile organic compounds (VOCs), which have been scrutinized as potential biomarkers for diagnosing acute exacerbation in diseased lungs. However, the pathogenic roles of VOCs in mucus dysregulation are unknown. By using air-liquid interface cultures of normal and diseased human bronchial epithelial cells and a mouse model of chronic VOCs exposure, we report that dominant species of P. aeruginosa VOCs in concentrations found in both the breath of cystic fibrosis patients and in the headspace of bacterial cultures significantly elevated the expression of the mucin MUC5AC. VOCs activate the AhR signaling to inhibit FOXA2, a key regulator of airway mucus homeostasis. AhR inhibitor restored FOXA2 expression to attenuate excessive mucin expression. Mechanistic studies revealed that P. aeruginosa VOCs activate the AhR-ARNT-CYP1-ROS signaling cascade, which in turn induces the EGFR-AKT/ERK signaling pathways to disrupt airway mucus homeostasis. Taken together, these findings highlight the critical role of P. aeruginosa VOCs in disrupting airway mucus homeostasis and implicate the pathogenic role of AhR signaling in chronic lung diseases. - Source: PubMed
Publication date: 2026/08/10
Kuo Shanny HsuanLew Shi QianChong Sook YinWu CongWilliams Allison BKosmider BeataRandell Scott HRahme Laurence GLau Gee W - Holistic protection goals in environmental hazard and risk assessment, complex pollutant mixtures, and limitations in targeted chemical analysis highlight the need for robust, mechanistically informative bioanalytics to support water quality monitoring. Given the scarcity of high-throughput, non-mammalian in vitro effect-based methods, this study evaluates the suitability of mammalian models as surrogates for aquatic species by investigating interspecies differences in the activation of oxidative stress (Nrf2/Keap1/ARE) and xenobiotic metabolism (AhR/ARNT/XRE) pathways quantified with cellular reporter gene assays. Wastewater treatment plant influent and effluent samples, alongside reference compounds, were analysed in human, mouse, and zebrafish reporter assays. Bioanalytics were complemented by in silico-mediated effect-directed analysis, iceberg-, molecular docking-, and chemical bioavailability-modelling. For Nrf2/Keap1/ARE, high concordance in reporter activity across species was observed in response to environmental samples, whereas the reference compound tert-butylhydroquinone elicited species-/assay-specific differences due to varying ligand affinities for the Keap1 redox sensor. In contrast, metazachlor exposure resulted in conserved activation patterns across species. For AhR/ARNT/XRE, interspecies variability in bioactivity was observed across environmental samples and the reference compound 2,3,7,8-tetrachlorodibenzodioxin, yielding divergent bioequivalent concentration estimates. In silico-mediated effect-directed analysis identified climbazole, daidzein, and thiabendazole as principal aryl hydrocarbon receptor activators, which also displayed species-/assay-specific activity under isolated exposure. Molecular docking confirmed species-dependent receptor-ligand affinities, while bioavailability modelling excluded differential cellular uptake, supporting receptor-mediated mechanisms as key drivers. Collectively, mammalian reporter assays can approximate oxidative stress responses in aquatic species, but limitations remain for xenobiotic metabolism, highlighting the need for species-representative assays and caution when contextually interpreting data from mammalian systems. - Source: PubMed
Publication date: 2026/09/04
Lungu-Mitea SebastianMandava GeetaHoráčková JanaGolovko OksanaToušová ZuzanaBednář DavidAhrens LutzHilscherová KláraLundqvist Johan - Caffeine, a widely consumed psychoactive substance, has known effects on physiological and behavioral processes. Recent studies report that caffeine can influence the circadian rhythm, which is linked to many aspects of physiology, energy metabolism, and homeostasis. Therefore, we examined the arousal effects of caffeine via behavioral tests and assessed its impact on the circadian rhythm by measuring clock gene and clock-controlled gene expression in the brains of mice and Neuro 2a (N2a) cells. - Source: PubMed
Park SookyoungKhan Zeeshan AhmadAnsari AbuZarShamali Urala Kalasi ApsaraKar Anik KumarLee YejinLee GwangbaeKim JaeyeongSon SeminHong Yonggeun - The development of Alzheimer disease (AD) involves a cluster of pathogenic processes, including amyloid-beta (Aβ) deposition, tau-mediated neurodegeneration, chronic neuroinflammation, oxidative stress (OS), metabolic dysregulation, and disruption of circadian rhythms. Nuclear hormone receptor, Retinoic Acid-Related Orphan Receptor Alpha (RORα) was shown to regulate multiple neuroprotective pathways such as inflammatory signaling (NF-κB suppression), mitochondrial integrity and mitophagy, redox homeostasis [upregulation of glutathione peroxidase 1 (GPX1), and mitochondrial superoxide dismutase 2, (SOD2)], calcium-dependent synaptic architecture [inositol 1,4,5-trisphosphate receptor type 1 (ITPR1), Purkinje cell protein 4 (PCP4)], and circadian rhythm stability [period 2 (PER2), brain and muscle ARNT-like 1 (BMAL1)]. Multi-omics network analyses place RORα within regulatory networks that are co-associated with key AD-related genes and supports an associational, network-based relationship for . Preclinical gene-augmentation studies using adeno-associated viral vectors report that RORα overexpression reduces APP levels, remodels the complement regulator CD59 glycoprotein (CD59), inhibits OS, and enhances neuronal survival, although these effects were established largely in retinal and other non-AD systems. These findings support the potential of as a therapeutic target through genetic intervention, but direct demonstration of AD-modifying efficacy is still lacking. Investigational -focused gene therapy in retinal degenerative diseases provides proof-of-concept for, but does not yet establish, applicability within the central nervous system. Taken together, this evidence nominates as a candidate system-level regulator that may help restore disrupted homeostatic transcriptional networks in AD, a hypothesis that remains to be tested. We propose that RORα functions as a transcriptional hub coupling three homeostatic axes that fail in AD; the circadian, mitochondrial-metabolic, and immune-inflammatory axes, and that its regional expression changes in AD (hippocampal up-regulation vs. suprachiasmatic down-regulation) represent a compensatory response that ultimately fails. Cell-type-specific expression profiling is required to determine in which regions augmentation may be therapeutically appropriate. Restoring RORα is therefore could be network-stabilizing rather than single-pathway intervention. - Source: PubMed
Publication date: 2026/08/20
Chintalapally ShivakanthRajanala KalpanaUpadhyay Arun - Chronic atrophic gastritis (CAG) is a critical precancerous stage in the development of gastric cancer (GC). Circadian rhythm disruption perturbs the core clock gene network, including circadian locomotor output cycles kaput (), brain and muscle ARNT-like 1 (), period circadian protein homolog (), and cryptochrome (). These alterations contribute to a multi-layered pathological cascade involving DNA damage accumulation, epigenetic remodeling, altered epithelial cell plasticity, cellular senescence, microbiota dysbiosis, tumor microenvironment remodeling, metabolic reprogramming, aberrant angiogenesis, and dysregulated cell death, thereby accelerating CAG to GC progression. However, existing studies have predominantly treated the circadian rhythm as a passive risk factor for disease onset and have yet to elevate it to an actionable interventional target within the full-course management of gastric precancerous lesions. Building on a systematic synthesis of the mechanistic evidence outlined above, this review proposes a predictive, preventive and personalised medicine (PPPM/3PM) three-tier management framework grounded in circadian-based individualised protection. At the predictive level, digital biomarkers (sleep-wake rhythms, light exposure, physical activity, and dietary behavior), multi-omics profiles, and circadian-related molecular signatures are integrated to achieve dynamic risk stratification of CAG populations. At the targeted prevention level, pharmacological agents and natural compounds with circadian-regulating potential are deployed to develop proactive protective strategies tailored to distinct pathological stages and circadian phenotypes. At the personalised treatment level, lifestyle interventions, chronotherapy, nano-carrier-based circadian-synchronised delivery, and dynamic biomarker monitoring are combined to formulate precision intervention regimens informed by individual circadian phenotypes. This framework repositions the circadian rhythm from a latent risk factor to a protectable and therapeutically targetable axis, offering new insights into time-optimised intervention strategies for the inflammation to cancer transition in CAG. - Source: PubMed
Publication date: 2026/08/21
Shan CengGuo MinFeng FeifanWang XihongLi MohangXu WeichaoJia KeyuLiu YifeiJia Yifan