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ToxSci Advance Access originally published online on October 16, 2008
Toxicological Sciences 2008 106(2):301-303; doi:10.1093/toxsci/kfn220
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© The Author 2008. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Ah Receptor Binding to its Cognate Response Element is Required for Dioxin-Mediated Toxicity

Gary H. Perdew1

Center for Molecular Toxicology and Carcinogenesis and the Department of Veterinary and Biomedical Sciences, Pennsylvania State University, University Park, Pennsylvania 16802

1 To whom correspondence should be addressed at Center for Molecular Toxicology and Carcinogenesis, Pennsylvania State University, 309 LSB, University Park, PA 16802. Fax: (814)-863-1696. E-mail: ghp2@psu.edu.

Received October 7, 2008; accepted October 8, 2008

The first 150 words of the full text of this article appear below.

The aryl hydrocarbon receptor (AHR) is a ligand-activated member of the bHLH-PAS family of transcription factors. Members of this family include HIF1{alpha}, EPAS, and SIM, which are involved in hypoxia and nervous system development. Another member of this family, aryl hydrocarbon nuclear translocator (ARNT), is the dimerization partner for the AHR. The AHR is often classified as a sensor of a wide range of xenobiotics, leading to induction of xenobiotic metabolism through enhanced expression of phase I/II enzymes. The environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a prototypic ligand for the AHR and is often used to study the effects of prolonged AHR activation. Rodent exposure to TCDD results in a plethora of toxic effects, including wasting syndrome, tumor promotion, developmental defects, and liver toxicity (reviewed in Vanden Heuvel and Lucier, 1993Go). The key target genes that lead to these toxic end points are largely unknown. AHR activation . . . [Full Text of this Article]

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