Another important biological function for the aryl hydrocarbon receptor.

For many years, the aryl hydrocarbon receptor (AhR) had been studied primarily for its contribution to environmental chemical-induced organ toxicity or carcinogenicity.1–3 The prevailing paradigm fashioned from these studies held that activation of the cytosolic AhR by any one of a variety of environmental pollutants (eg, planar polychlorinated biphenyls, polycyclic aromatic hydrocarbons, and dioxins) results in nuclear AhR translocation and transcriptional upregulation of prototypic target genes encoding cytochrome P450 enzymes (eg, CYP1A1 and CYP1B1).4–6 These enzymes are capable of metabolizing at least some of the environmental AhR ligands into toxic or mutagenic intermediates, thereby affecting biological outcomes. Although these studies were extremely important for defining the AhR as an environmental ligand-induced transcription factor and in mapping out portions of the AhR signaling pathway, they did not directly provide evidence of the “normal” physiological function of …

[1]  O. Fiehn,et al.  Activation of Aryl Hydrocarbon Receptor Induces Vascular Inflammation and Promotes Atherosclerosis in Apolipoprotein E−/− Mice , 2011, Arteriosclerosis, thrombosis, and vascular biology.

[2]  H. Weiner,et al.  An endogenous aryl hydrocarbon receptor ligand acts on dendritic cells and T cells to suppress experimental autoimmune encephalomyelitis , 2010, Proceedings of the National Academy of Sciences.

[3]  Xiaoqing Chang,et al.  The aryl hydrocarbon receptor binds to E2F1 and inhibits E2F1-induced apoptosis. , 2008, Molecular biology of the cell.

[4]  J. Buer,et al.  The aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to environmental toxins , 2008, Nature.

[5]  D. Seldin,et al.  Green tea polyphenols reverse cooperation between c-Rel and CK2 that induces the aryl hydrocarbon receptor, slug, and an invasive phenotype. , 2007, Cancer research.

[6]  F. Matsumura,et al.  RelB, a new partner of aryl hydrocarbon receptor-mediated transcription. , 2007, Molecular endocrinology.

[7]  H. Swanson,et al.  Lack of the Aryl Hydrocarbon Receptor Leads to Impaired Activation of AKT/Protein Kinase B and Enhanced Sensitivity to Apoptosis Induced via the Intrinsic Pathway , 2007, Journal of Pharmacology and Experimental Therapeutics.

[8]  J. Reiners,et al.  Aryl Hydrocarbon Receptor Modulation of Tumor Necrosis Factor-α-induced Apoptosis and Lysosomal Disruption in a Hepatoma Model That Is Caspase-8-independent* , 2006, Journal of Biological Chemistry.

[9]  G. Sonenshein,et al.  7,12-dimethylbenz(a)anthracene treatment of a c-rel mouse mammary tumor cell line induces epithelial to mesenchymal transition via activation of nuclear factor-kappaB. , 2006, Cancer research.

[10]  A. Akintobi,et al.  2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces matrix metalloproteinase (MMP) expression and invasion in A2058 melanoma cells. , 2006, Toxicology and applied pharmacology.

[11]  N. Kerkvliet,et al.  Cutting Edge: Activation of the Aryl Hydrocarbon Receptor by 2,3,7,8-Tetrachlorodibenzo-p-dioxin Generates a Population of CD4+CD25+ Cells with Characteristics of Regulatory T Cells1 , 2005, The Journal of Immunology.

[12]  P. A. Pérez-Mancera,et al.  Immortalized Mouse Mammary Fibroblasts Lacking Dioxin Receptor Have Impaired Tumorigenicity in a Subcutaneous Mouse Xenograft Model* , 2005, Journal of Biological Chemistry.

[13]  H. Swanson,et al.  Dioxin-induced Immortalization of Normal Human Keratinocytes and Silencing of p53 and p16INK4a* , 2004, Journal of Biological Chemistry.

[14]  F. Bibeau,et al.  Roles of the Transcription Factors Snail and Slug During Mammary Morphogenesis and Breast Carcinoma Progression , 2004, Journal of Mammary Gland Biology and Neoplasia.

[15]  Stephen Safe,et al.  Aryl hydrocarbon receptor gene silencing with small inhibitory RNA differentially modulates Ah-responsiveness in MCF-7 and HepG2 cancer cells. , 2003, Molecular pharmacology.

[16]  Matthew W. Strobeck,et al.  Role of the aryl hydrocarbon receptor in cell cycle regulation. , 2002, Toxicology.

[17]  M. Nagarkatti,et al.  2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces Fas-dependent activation-induced cell death in superantigen-primed T cells , 2002, Archives of Toxicology.

[18]  S. Korsmeyer,et al.  Aromatic hydrocarbon receptor-driven Bax gene expression is required for premature ovarian failure caused by biohazardous environmental chemicals , 2001, Nature Genetics.

[19]  A. Fornace,et al.  Altered cell cycle control at the G(2)/M phases in aryl hydrocarbon receptor-null embryo fibroblast. , 2000, Molecular pharmacology.

[20]  M. E. Hahn.  The aryl hydrocarbon receptor: a comparative perspective. , 1998, Comparative biochemistry and physiology. Part C, Pharmacology, toxicology & endocrinology.

[21]  J. Whitlock,et al.  The aromatic hydrocarbon receptor modulates the Hepa 1c1c7 cell cycle and differentiated state independently of dioxin , 1996, Molecular and cellular biology.

[22]  G. Perdew,et al.  Subunit composition of the heteromeric cytosolic aryl hydrocarbon receptor complex. , 1994, The Journal of biological chemistry.

[23]  D. Nebert,et al.  Human AH locus polymorphism and cancer: inducibility of CYP1A1 and other genes by combustion products and dioxin. , 1991, Pharmacogenetics.

[24]  O. Hankinson.  Dominant and recessive aryl hydrocarbon hydroxylase-deficient mutants of mouse hepatoma line, Hepa-1, and assignment of recessive mutants to three complementation groups , 1983, Somatic cell genetics.

[25]  D. Nebert,et al.  Genetic expression of aryl hydrocarbon hydroxylase activity. Induction of monooxygenase activities and cytochrome P1-450 formation by 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice genetically "nonresponsive" to other aromatic hydrocarbons. , 1974, The Journal of biological chemistry.

[26]  Nebert Dw,et al.  Genetic regulation of aryl hydrocarbon hydroxylase induction in the mouse. , 1972 .

[27]  F. Matsumura,et al.  Activation of inflammatory mediators and potential role of Ah-receptor ligands in foam cell formation , 2007, Cardiovascular Toxicology.

[28]  W. Foster,et al.  Benzo-[a]-pyrene increases invasion in MDA-MB-231 breast cancer cells via increased COX-II expression and prostaglandin E2 (PGE2) output , 2005, Clinical & Experimental Metastasis.

[29]  C. Bradfield,et al.  Purification and N-terminal amino acid sequence of the Ah receptor from the C57BL/6J mouse. , 1991, Molecular pharmacology.

[30]  D. Nebert,et al.  Genetic regulation of aryl hydrocarbon hydroxylase induction in the mouse. , 1972, Federation proceedings.