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
- Circadian clocks strongly influence adipocyte biology. Studying adipocyte circadian regulation in the absence of organismal cues isolates cell-autonomous clock control, providing insight into mechanisms relevant to metabolic disease. To resolve circadian core biological programs, we deeply sequenced bulk RNA from inguinal-derived, in vitro-differentiated adipocytes (IVDAs) over a 2.5-day circadian time-course and compared clock-controlled genes (CCGs) with existing mouse supraclavicular brown adipose tissue (BAT) and epididymal white adipose tissue (eWAT) circadian time-course datasets. Using Phase Set Enrichment Analysis (PSEA), we report that 21% of the protein-coding transcriptome is rhythmic in IVDAs. Intrinsic circadian regulation governs key processes in energy metabolism, molecular transport, and transcription. Integration with in vivo datasets reveals that BAT and IVDAs exhibit more cohesive rhythmic pathways than does eWAT, clustering around the late-night early-morning transition. To explore how these pathways may be regulated, we reexamine a recent interscapular BAT cistrome dataset. Using in vitro-differentiated adipocyte (IVDA) transcription factors that are phase-aligned (≤4 h) with in vivo as input, motif enrichment analysis reveals 2 temporally distinct regulatory programs: an early E-box activator ARNT-family/bHLH-PAS program is enriched for transcriptional regulation, RNA metabolism, and signaling pathways, and a late nuclear receptor-associated program is enriched for energy metabolism, phospholipid biosynthesis, mitochondrial function, extracellular matrix (ECM) organization, and nuclear receptor signaling. Overall, we identify novel rhythmic transcripts and define cell-autonomous circadian programs in adipocytes whose timing is further sculpted by systemic cues in vivo. Because obesity is associated with adipocyte hypertrophy and hyperplasia, processes likely influenced by circadian regulation, these findings advance our understanding of clock-controlled adipocyte metabolism and its contribution to metabolic dysfunction. - Source: PubMed
Publication date: 2026/09/15
Worthen Jennifer MFrederick Armina-Lyn MDumesic Phillip ALoros Jennifer JDunlap Jay C - Bioanalytical methods targeting adverse cellular outcomes are increasingly used in environmental toxicology, including receptor-mediated toxicity pathways relevant to high-throughput monitoring of drinking water, wastewater, and other environmental samples. However, despite their increasing regulatory acceptance, the representativeness of human tissue-derived bioassays for assessing toxicity toward aquatic species remains uncertain. Given these circumstances, this data article presents molecular docking and sequence-alignment datasets generated to compare human and zebrafish receptor/sensor variants associated with the oxidative stress response (Keap1/Nrf2) and xenobiotic metabolism (AhR/ARNT) pathways. The dataset includes docking data for hKeap1, zfKeap1a, and zfKeap1b, as well as hAhR, zfAhR1a, zfAhR1b, and zfAhR2 receptor/sensor variants, with selected reference ligands and environmental pollutants. Receptor/sensor protein structures derived from AlphaFold predictions, X-ray crystallography, or cryo-electron microscopy were retrieved, prepared, and refined for molecular docking. Ligand structures included the reference agonists tetrachlorodibenzodioxin and tert‑butylhydroquinone, as well as the environmental pollutants climbazole, daidzein, thiabendazole, and metazachlor. Docking was performed using AutoDock Vina, generating the best-energy poses for each ligand-protein pair within defined docking grids. AlphaFold-predicted structures were evaluated by parallel docking into available partial X-ray crystal structures of the corresponding variants. For Keap1 variants, blind and site-directed docking approaches were applied, including grids covering reactive cysteine-associated binding regions, and potential effects of Keap1 dimerisation were considered. For AhR variants, docking focused on the PAS-B ligand-binding domain. Protein sequence alignment was conducted using the ClustalW algorithm to compare human and zebrafish receptor/sensor variants and support cross-species comparison of docking outputs. The dataset comprises prepared protein and ligand files, representative docking poses, binding-affinity outputs, and sequence-alignment data. These files provide reusable input and output material for comparative toxicology, cross-species extrapolation, receptor-ligand interaction assessment, and benchmarking of molecular docking workflows. The data may inform scientists and regulators interested in molecular initiating events, toxicity-pathway conservation, and interspecies differences in receptor-mediated responses. This data article complements a related research article by providing supporting docking data, receptor/sensor variant sequence-alignments, and quality-assurance procedures for the molecular docking workflow. - Source: PubMed
Publication date: 2026/07/07
Lungu-Mitea SebastianHoráčková JanaBednář DavidHilscherová Klára - Venetoclax (VEN) resistance remains a major obstacle to durable responses in acute myeloid leukemia (AML). Although the core circadian regulator brain and muscle ARNT-like protein 1 (BMAL1) has been implicated in AML progression and drug response, its role in acquired VEN resistance remains unclear. In this study, VEN-resistant R-THP1 and R-MOLM13 cells were established, and the role of BMAL1 was evaluated using public datasets, clinical samples, cell experiments, and in vivo xenograft models. BMAL1 was upregulated in relapsed/refractory AML samples and VEN-resistant cells, and high BMAL1 expression was associated with adverse clinical outcomes. BMAL1 knockdown increased VEN sensitivity, promoted apoptosis, and reduced proliferation and clonogenic capacity in resistant cells, whereas BMAL1 overexpression produced the opposite effects in parental cells. Consistently, BMAL1 depletion reduced leukemia burden and enhanced the response to VEN in vivo. Integrated transcriptomic and proteomic analyses identified tumor protein D52 (TPD52) as a downstream candidate associated with BMAL1-mediated VEN resistance. TPD52 was upregulated in resistant AML cells, and its genetic modulation recapitulated the effects of BMAL1 on VEN sensitivity and malignant phenotypes of AML. Co-immunoprecipitation supported an association between BMAL1 and TPD52, while cycloheximide chase assays showed that BMAL1 enhanced TPD52 protein stability. Modulation of BMAL1 or TPD52 also altered p-PI3K and p-AKT without markedly affecting on total PI3K or AKT expression. In conclusion, these findings indicate that BMAL1 contributes to acquired VEN resistance by interacting with and stabilizing TPD52, accompanied by PI3K/AKT activation. BMAL1-TPD52 axis maybe a novel therapeutic target to overcome VEN resistance in AML. - Source: PubMed
Publication date: 2026/09/11
Li SongyangYang YongjieLiu DongmeiHuang MeixiaLi JiayaoDu YinxiaoQin ZifeiLiu XiaomeiHuang NingYang Jing - The cellular export of large-sized proteins, such as collagen or fibrillin, necessitates a specialized transport pathway tailored towards their size. For collagen and possibly also other bulky proteins, the Transport ANd Golgi Organization 1 (TANGO1) protein plays a substantial role in the transfer from the Endoplasmic Reticulum (ER) to the Golgi apparatus. TANGO1 and related proteins organize the ER exit sites and generate large export structures within the cytosol while anchored to the ER membrane. In contrast to other proteins involved, TANGO1 features a folded domain in the ER lumen, which seems to be central for detecting cargos. This cargo-recognition domain has been shown to bind the collagen-specific chaperone HSP47 (Ishikawa et al. 2016) as well as type IV collagen directly (Arnolds and Stoll 2023). However, the exact molecular mechanism of these interactions remains unknown. The resonance assignments presented here lay the foundation for the experiments studying the binding process on a molecular level and is designed to facilitate investigations into how TANGO1 detects and selects the cargos to be exported. - Source: PubMed
Publication date: 2026/09/11
Auch JelenaPeddinghaus Anna CarlottaStoll Raphael - 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