High impact information on AHR

• Antiproliferative and antiangiogenic effects of 3-methylcholanthrene, an aryl-hydrocarbon receptor agonist, in human umbilical vascular endothelial cells [1].
• The results suggest that the adverse effects of 3-MC are mainly mediated by the aryl hydrocarbon receptor and not via increased oxidative stress [1].
• Although the expression of aryl hydrocarbon receptor (AHR) as well as the partner molecule, AHR nuclear translocator (ARNT) in the brain has been reported, the effect of TCDD on the brain remains to be clarified in detail [2].
• Role of aryl hydrocarbon receptor in mesencephalic circulation failure and apoptosis in zebrafish embryos exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin [2].
• Measurement of [3H]TCDD uptake and Ah receptor binding indicated that the apparent difference in potencies was a result of decreased bioavailability in the presence of serum, effectively reducing the concentration of TCDD within the cells [3].

Biological context of AHR

• Neither AHR mRNA nor protein expression varied during the cell cycle, as measured by RT-PCR and specific binding of [(3)H]TCDD in synchronous PLHC-1 cells [4].
• The specific objectives were to characterize proliferation rates and the cell cycle in these cells, to measure effects of TCDD on cell proliferation, and to determine if expression of the AHR varies during the cell cycle [4].
• The overall objective of the present work was to investigate possible interactions between cell proliferation, the cell cycle, and AHR signal transduction in a piscine system, the PLHC-1 cell line, which is being used increasingly in aquatic toxicological research [4].

Associations of AHR with chemical compounds

• Aryl hydrocarbon receptor (AHR) ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) cause altered cell proliferation in many tissues in vivo and cell types in vitro, and the AHR has been suggested to play a role in cell cycle regulation in mammalian systems [4].

References