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hypoxia is capable of promoting the Th17 response by reducing AhR activity via HIF-1alpha activity.
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This review will discuss the growing body of literature that provides evidence that the AhR protects the lungs against the damaging effects of cigarette smoke.
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Results show that environmentally persistent free radicals (EPFR) increase aryl hydrocarbon receptor activation and reactive oxygen species (ROS) production in human bronchial epithelial cells. While AhR activation was correlated with an increased expression of oxidant-producing enzymes, it is possible that AhR activation is both a cause and effect of EPFR-induced ROS.
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Mutant AHR failed to promote 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD)-induced xenobiotic responsive element (XRE) luciferase activity. In parallel, mutation in AHR abolished activation of its downstream target gene, such as CYP1A1 and CYP1A2
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we found a constitutive nuclear localization of AhR in every placental model, in the absence of any voluntarily-added exogenous activator. Our data suggest an intrinsic activation of AhR due to the presence of endogenous placental ligands.
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AHR protein levels were upregulated in all grades of meningioma compared to control meninges. As the grade of the meningioma progresses from low to high grade we also observed that AHR protein levels were upregulated significantly, indicating an important role of AHR in meningioma tumor progression.
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The aim of this study was to investigate serum concentrations of AhR, cytochromes P450 (CYP) 1A1 and 1B1 in patients with exacerbated psoriasis vulgaris.
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AhR p.Arg554Lys polymorphism, alone and in combination with parental exposures, is associated with the congenital heart disease risk.
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AhR is higher expressed in short androgen receptor (AR) poly-glutamine polymorphism (AR-Q) tumour compared to that in long AR-Q patient.
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This study evaluated the mechanism by which p23 triggers degradation of AHR, and the role of HSP90 in this process.
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The compound leads, 4-Me-indole and 7-MeO-indole, induced substantial nuclear translocation of the AhR.
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To study the potential role of AHR pathway in CML progenitors and stem cells, we have first evaluated the expression of AHR in UT-7 cell line expressing BCR-ABL. AHR expression was highly reduced in UT-7 cell expressing BCR-ABL as compared to controls.
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Altogether, our data suggest that a transcriptional defect of AhR could be a susceptibility factor for the development of vitiligo.
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AhR activation in macrophages causes a block to HIV-1 and HSV-1 replication.
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These findings suggest that Malassezia pachydermatis infection of human keratinocytes induces activation of the AhR, and increases the expression of its responsive genes, including CYP1A1.
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The author's observations point to a possible effect of local AhR ligands in the regulation of the function of CD56(bright) tissue-resident or intratumoral NK cells.
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AHR pathway is activated both in chronic kidney disease and could be a key mechanism involved in the deleterious cardiovascular effects observed in CKD.
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Expression of microRNA potentially regulated by AhR and CAR in malignant tumors of the endometrium has been reported.
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The overexpression and activation of AHR are involved in the early development of skin squamous cell carcinomas. AHR expression correlates with EGFR expression and may influence cell proliferation.
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These studies identified SNPs that were cis-eQTLs for DEFB1 and AHR and, which were associated with variation in plasma KYN concentrations that were related to severity of major depressive disordersymptoms.
