Abstract
For more than 30 years, the aryl hydrocarbon receptor [Ah receptor (AHR)] has been extensively scrutinized as the cellular receptor for numerous environmental contaminants, including polychlorinated dioxins, dibenzofurans, and biphenyls. Recent evidence argues that this description is incomplete and perhaps myopic. Ah receptor orthologs have been demonstrated to mediate diverse endogenous functions in our close vertebrate relatives as well as our distant invertebrate ancestors. Moreover, these endogenous functions suggest that xenobiotic toxicity may be best understood in the context of intrinsic AHR physiology. In this literature review, we survey the emerging picture of endogenous AHR biology from work in the vertebrate and invertebrate model systems Mus musculus, Caenorhabditis elegans, and Drosophila melanogaster.
Footnotes
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This work was supported by National Institutes of Health grants R37-ES05703, T32-CA009135, and P30-CA014520
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Article, publication date, and citation information can be found at http://molpharm.aspetjournals.org.
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doi:10.1124/mol.107.037259.
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ABBREVIATIONS: AHR, aryl hydrocarbon receptor; Ah, aryl hydrocarbon; bHLH, basic helix-loop-helix; PAS, Per-ARNT-Sim; TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin; LOF, loss of function; ARNT, aryl hydrocarbon receptor nuclear translocator; DRE, dioxin response element; Hsp90, 90-kDa heat shock protein; RME, ring motor neuron; PNS, peripheral nervous system; da, dendritic arborization; PR, photoreceptor cell; Rh, rhodopsin; LDL, low-density lipoprotein; TGF-β, transforming growth factor-β; LTBP, latent TGF-β binding protein.
- Received April 18, 2007.
- Accepted May 29, 2007.
- The American Society for Pharmacology and Experimental Therapeutics
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