Ask about this productRelated 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
- The survival of nonvertebrate species that lack adaptive immunity has prompted the discovery of memory mechanisms in innate immune cells, termed trained immunity. Because infants depend on innate immunity to fight off pathogens, leveraging these mechanisms in neonatal care may hold clinical significance. Yet, this is constrained by limited understanding of innate immune memory development during early-life. By performing systems-level characterization of β-glucan-trained monocytes from adults, term infants, and preterm infants, we report maturation-dependent constraints in trained immunity. We corroborate these findings in a small cohort of premature infants with in utero pathogen exposure. Alongside limited stimulus-induced reprogramming of innate immune responses in the clinical cohort, monocytes from premature infants exhibited metabolic alterations in glutaminolysis and tricarboxylic acid cycle metabolism, pathways central to trained immunity. They also displayed a treatment-robust long noncoding RNA landscape and transcriptional alterations in enzymes relevant to epigenetic induction of innate immune memory. Finally, network-based analyses implicated SMAD5 and ARNT as potential drivers of differences and provided evidence for altered transcriptional regulation of chromatin organization across early-life development. Our results suggest that metabolic and transcriptomic immaturity constrains trained immunity in premature infants, highlighting a developmental mechanism that may affect host defense and guide future immunomodulatory strategies. - Source: PubMed
Publication date: 2026/10/04
Eigenschink MichaelDavogg ElsaPristner ManuelSeki DavidArzmüller MarcusKiss HerbertFarr AlexBerger AngelikaBerry DavidWarth BenediktWisgrill Lukas - Abnormal skin pigmentation is one of the most common skin conditions worldwide. The search for safe, effective, and well-tolerated skin-whitening agents remains a major challenge for the pharmaceutical and cosmetics industries. Glabridin (Gla), often referred to as the "whitening gold", is widely recognized as one of the most potent natural skin-whitening ingredients. However, its low bioavailability, poor skin permeability, and poor stability severely limit its efficacy in conventional topical formulations. Various studies have shown that glycyrrhizic acid (GA), as a drug carrier, can significantly improve the solubility, stability, and bioavailability of poorly soluble drugs, and the nanoparticles made from it have great potential. In this study, we propose using GA to encapsulate Gla, employing a "combined excipient and active ingredient" approach to improve the solubility, water dispersibility, and stability of Gla, thereby enhancing its transdermal delivery efficiency. After encapsulation, the size of the micelles was only about 37 nm, the encapsulation efficiency reached up to 80%, and the cumulative penetration over 48 h reached 7.44 μg/cm. The micelles also inhibit melanin production and reduce tyrosinase activity. Compared with a simple physical mixed solution or using Gla alone, high-concentration micelles reduced the expression of tyrosinase (TYR) to 0.2, tyrosinase-related protein-1 (TRP-1) to 0.6, and tyrosinase-related protein-2 (TRP-2) to 0.3. At the same time, they downregulated the expression of α-melanocyte-stimulating hormone (α-MSH), cyclic adenosine monophosphate (cAMP), and microphthalmia-associated transcription factor (MITF); and downregulated the Brain and Muscle ARNT-Like 1 (BMAL1) expression whilst upregulating the Period Circadian Regulator 1 (PER1) expression. This study demonstrates that GA-Gla micelles exert a synergistic effect by simultaneously targeting classical skin-whitening pathways and circadian regulatory networks, indicating great potential for skin whitening and providing a new strategy for developing novel, highly effective skin-whitening agents. - Source: PubMed
Publication date: 2026/10/01
Ni LehuanLuo MingLiu JiaxinZeng MinghuiZeng LijuanJenis JanarJi HaoXia HonglinLuo ShilinYan YongtaoChen YaLiu LiWu YugeFeng YongshiLi JiansenPeng YiquanZhu HongxiaWang ZhuxianLiu Qiang - The aryl hydrocarbon receptor (AHR) and the vitamin D receptor (VDR) were long regarded as independent transcription factors governing distinct physiology-xenobiotic sensing and calcium-vitamin D homeostasis, respectively. AHR, a basic helix-loop-helix/PAS protein, heterodimerizes with ARNT and binds xenobiotic response elements (XREs) to drive cytochrome P450 genes such as ; VDR, a nuclear receptor activated by 1,25-dihydroxyvitamin D, heterodimerizes with RXR and binds vitamin D response elements (VDREs). Although their genes reside on separate chromosomes (, Chr 7; , Chr 12), an integrated view recognizes the two pathways as extensively cross-regulatory. This review synthesizes the molecular, immunological, and tissue-level evidence for VDR-AHR interplay. At the molecular level, the receptors cooperate at composite promoter architectures-most notably an everted-repeat VDRE positioned adjacent to an XRE in the promoter-while AHR ligands reciprocally enhance -mediated catabolism of active vitamin D. Tryptophan metabolism provides a bidirectional hub: kynurenine and the UVB photoproduct FICZ serve as endogenous AHR ligands whose balance, modulated by VDR, shapes signaling output. The tumor suppressor p53 functions as a shared upstream regulator coupling genotoxic stress to both receptors, with convergence on the (p21) checkpoint. Functionally, AHR and VDR converge on the regulatory T cell (Treg)/Th17 axis to influence immune tolerance: sustained AHR activation by TCDD favors Foxp3 Treg differentiation, transient FICZ-driven activation promotes Th17 responses, and VDR reinforces the tolerogenic arm while independently repressing IL-17. The receptors further cooperate in maintaining intestinal epithelial barrier integrity and NF-κB restraint, with parallel impairment in inflammatory bowel disease, and are co-activated in skin by solar UVB, which simultaneously generates vitamin D and the AHR ligand FICZ within keratinocytes. In cancer, VDR acts as a tumor suppressor, AHR exhibits context-dependent pro- and anti-tumor roles, and a three-way AHR-VDR-p53 interaction-inverted by mutant p53-forms a critical regulatory node. Throughout, the direction and magnitude of cross-talk prove highly dependent on cell type, ligand identity and kinetics, and species-distinctions often underappreciated in the literature. Clarifying these context-specific determinants is essential for translating AHR-VDR cross-regulation into rational therapies in autoimmunity, mucosal inflammation, dermatology, and oncology. - Source: PubMed
Publication date: 2026/09/08
Alqahtani Mohammed A - Di(2-ethylhexyl) phthalate (DEHP) and diisononyl phthalate (DiNP) are plasticizers used in many consumer products. Both phthalates alter estrous cyclicity, fertility indices, and folliculogenesis throughout the reproductive lifespan. Our companion paper showed that exposure to a phthalate mixture containing DEHP and DiNP altered the aryl hydrocarbon receptor (AHR) signaling pathway in the ovary. However, limited information was available on how DEHP and DiNP individually affect the AHR signaling pathway in the ovary throughout reproductive aging. Thus, we hypothesized that DEHP and DiNP individually affect the gene and protein expression and localization associated with the AHR pathway throughout the reproductive lifespan. We treated adult female CD-1 mice with corn oil control or doses (0.15 ppm, 1.5 ppm, or 1500 ppm) of DEHP and DiNP in the diet for 1-12 months. Sera were used to measure circulating estradiol (E2) concentrations. The AHR pathway was assessed using quantitative PCR (qPCR) for gene expression, RNAscopeTM in situ hybridization for transcript localization, and immunohistochemistry for protein localization. Exposure to DEHP, but not DiNP, reduced serum E2 after 1 month compared to control. DEHP exposure increased Cyp1a1 expression and CYP1B1 localization in the ovary after 6 months compared to control. DiNP also increased Arnt expression and CYP1B1 localization in the ovary after 1 month compared to control. DiNP exposure decreased Ahr and Cyp1a1 expression as well as CYP1A1 localization in the antral follicle after 12 months compared to control. Overall, DEHP and DiNP both influence the ovarian AHR pathway, but at different time points and doses. - Source: PubMed
Publication date: 2026/09/25
Dean Angela ESantacruz-Márquez RamsésSafar Adira MLaws Mary JSeaton Taylor AMiller EstellaHuff JustinHall Lydia MFlaws Jodi A - Phthalates are plasticizers and solvents used in numerous consumer products. Exposure to a phthalate mixture (Mix) alters estrous cyclicity, fertility indices, ovarian follicle dynamics, and steroidogenesis. In cultured antral follicles, phthalates alter the aryl hydrocarbon receptor (AHR) pathway, which is known for estradiol (E2) and xenobiotic metabolism. However, how phthalates affect the AHR pathway in the ovary in vivo and how this pathway changes throughout the reproductive lifespan are unknown. Thus, we hypothesized that expression and localization of genes and proteins in the AHR pathway change throughout the reproductive lifespan and in response to Mix exposure. We exposed adult female CD-1 mice to corn oil control or varying doses (0.15 ppm, 1.5 ppm, or 1500 ppm) of Mix for 1-12 months. Sera and ovaries were collected at each time point. Sera were used to determine circulating E2 concentrations. The AHR pathway in the ovaries was examined using quantitative PCR (qPCR) for gene expression, RNAscopeTM in situ hybridization for transcript localization, and immunohistochemistry for protein localization. The AHR pathway was altered throughout the reproductive lifespan, with increased Cyp1a1 expression and decreased CYP1B1 localization in the ovary at 13 months of age. Circulating E2 decreased throughout aging. Mix exposure altered Arnt and Ahr expression after 1 and 12 months, respectively. Additionally, Mix exposure increased CYP1A1 localization after 6 months, with areas of increased staining intensity in the ovary. Overall, the AHR pathway was altered with reproductive aging, and Mix exposure affected the pathway over time. - Source: PubMed
Publication date: 2026/09/25
Dean Angela ESantacruz-Márquez RamsésSafar Adira MLaws Mary JSeaton Taylor AMiller EstellaHuff JustinHall Lydia MFlaws Jodi A