Promoter analysis of TCDD-inducible genes in a thymic epithelial cell line indicates the potential for cell-specific transcription factor crosstalk in the AhR response

Dioxin Receptor Deficiency Impairs Angiogenesis by a Mechanism Involving VEGF-A Depletion in the Endothelium and Transforming Growth Factor-β Overexpression in the Stroma

“…Light microscopy was done at room temperature on a Nikon E-400 microscope equipped with a Nikon L16 camera with a ϫ10 objective (0. reduced angiogenesis in AhR ϩ/ϩ mice under the same experimental conditions. The mechanism by which AhR modulates angiogenesis through VEGF is in large part unknown, although (63). Altogether, we propose that AhR expression in endothelial cells maintains the production of active VEGF isoforms, at least in part through HIF-1␣, and that alteration of such mechanism contributes to defective angiogenesis in AhR-null mice.…”

Dioxin Receptor Expression Inhibits Basal and Transforming Growth Factor β-induced Epithelial-to-mesenchymal Transition

“…In addition to the control of cell cycle and cell proliferation (28,41,42), cell adhesion and migration are recognized as important cellular functions requiring AhR activity (43). This assumption is partially based on in vitro studies using MCF-7 breast tumor cells (44 -46), thymocytes (4,12,47), and hematopoietic stem cells (48) treated with the potent exogenous AhR ligand dioxin. AhR is also involved in cell adhesion and migration under physiological conditions through cell type-specific mechanisms (6,49).…”

Mechanistic Insights into the Events That Lead to Synergistic Induction of Interleukin 6 Transcription upon Activation of the Aryl Hydrocarbon Receptor and Inflammatory Signaling

“…Although TCDD treatment has variable effects on IL6 production depending on the cell type (39,40), the mechanism by which activated AHR influences the IL6 gene and the complex in which it plays a role has not been fully studied. Our analysis of the IL6 promoter showed that the receptor binds 3 kb upstream but in ChIP analysis can be found closer to the transcription start site, as well.…”