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Gene Review

AHR  -  aryl hydrocarbon receptor

Gallus gallus

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Disease relevance of AHR

  • The mechanism of HAH toxicity involves altered gene expression subsequent to activation of the aryl hydrocarbon receptor (AHR), a basic helix-loop-helix-PAS transcription factor [1].
  • Thus, the spatial and temporal expression of AhR and Arnt suggests that the developing myocardium and cardiac septa are potential targets of TCDD-induced teratogenicity, and such targets are also consistent with cardiac hypertrophy and septal defects observed following TCDD exposure [2].
  • Since high levels of AhR ligands are found in cigarette smoke, and further since smoking is an important risk factor in both osteoporosis and periodontal disease, it may be postulated that AhR ligands are the component of cigarette smoke linking smoking to osteoporosis and periodontal disease [3].

High impact information on AHR

  • These studies provide a molecular understanding of species differences in sensitivity to dioxin-like compounds and suggest an approach to using the AHR as a marker of dioxin susceptibility in wildlife [1].
  • Here, we show that although chicken and tern AHRs both exhibit specific binding of [(3)H]TCDD, the tern AHR has a lower binding affinity and exhibits a reduced ability to support TCDD-dependent transactivation as compared to AHRs from chicken or mouse [1].
  • Cytochrome P-450-mediated arachidonic acid metabolism in chick embryo liver microsomes was increased by both Ah receptor-dependent (2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and beta-naphthoflavone) and independent (phenobarbital) P-450 inducers [4].
  • Although the heart is a principal target organ for TCDD toxicity and AhR is expressed throughout embryogenesis, induction of CYP1A was not observed in the chick heart [5].
  • In contrast with polychlorinated biphenyls, Ah receptor binding affinities of PBDEs could not be related to the planarity of the molecule, possibly because the large size of the bromine atoms expands the Ah receptor's binding site [6].

Chemical compound and disease context of AHR


Biological context of AHR

  • Phylogenetic analysis of these and other AHR amino acid sequences showed that the bird and mudpuppy AHRs were more closely related to mammalian and fish AHR1 forms than to fish AHR2 [10].
  • These data suggest that AhR ligands inhibit osteogenesis probably through inhibition of osteodifferentiation and that this effect can be antagonized by resveratrol [3].
  • Aryl hydrocarbon receptor (AhR) ligands are environmental contaminants found in cigarette smoke and other sources of air pollution [3].
  • The differential responses of chicken and Eider duck embryos were used to examine the involvement of Ah receptor-mediated enzyme induction in the activation of the environmental and food mutagen 3-amino- 1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) [11].
  • 2,3,7,8-Tetrachlorodibenzo-p-dioxin elicits aryl hydrocarbon receptor-mediated apoptosis in the avian DT40 pre-B-cell line through activation of caspases 9 and 3 [12].

Anatomical context of AHR


Associations of AHR with chemical compounds


Regulatory relationships of AHR


Other interactions of AHR

  • The developmental expression of CYP1A4-associated aryl hydrocarbon (benzo[a]pyrene) hydroxylase (AHH) activity and its association with expression of the Ah receptor had previously been characterized in chick embryo liver [19].

Analytical, diagnostic and therapeutic context of AHR

  • We further show through use of chimeric AHR proteins and site-directed mutagenesis that the difference between the chicken and tern AHRs resides in the ligand-binding domain and that two amino acids (Val-325 and Ala-381) are responsible for the reduced activity of the tern AHR [1].
  • Use of the gel retardation assay with a synthetic oligonucleotide indicated that in these cases the liganded Ah receptor failed to bind to the DNA recognition sequence [6].
  • Fate of Ah-receptor agonists in organic household waste during anaerobic degradation--estimation of levels using EROD induction in organ cultures of chick embryo livers [20].


  1. The molecular basis for differential dioxin sensitivity in birds: Role of the aryl hydrocarbon receptor. Karchner, S.I., Franks, D.G., Kennedy, S.W., Hahn, M.E. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  2. Expression of the aryl hydrocarbon receptor (AhR) and AhR nuclear translocator during chick cardiogenesis is consistent with 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced heart defects. Walker, M.K., Pollenz, R.S., Smith, S.M. Toxicol. Appl. Pharmacol. (1997) [Pubmed]
  3. Inhibition of dioxin effects on bone formation in vitro by a newly described aryl hydrocarbon receptor antagonist, resveratrol. Singh, S.U., Casper, R.F., Fritz, P.C., Sukhu, B., Ganss, B., Girard, B., Savouret, J.F., Tenenbaum, H.C. J. Endocrinol. (2000) [Pubmed]
  4. Beta-naphthoflavone induction of a cytochrome P-450 arachidonic acid epoxygenase in chick embryo liver distinct from the aryl hydrocarbon hydroxylase and from phenobarbital-induced arachidonate epoxygenase. Nakai, K., Ward, A.M., Gannon, M., Rifkind, A.B. J. Biol. Chem. (1992) [Pubmed]
  5. Biochemical and molecular biological analysis of different responses to 2,3,7,8-tetrachlorodibenzo-p-dioxin in chick embryo heart and liver. Kanzawa, N., Kondo, M., Okushima, T., Yamaguchi, M., Temmei, Y., Honda, M., Tsuchiya, T. Arch. Biochem. Biophys. (2004) [Pubmed]
  6. Synthesis of polybrominated diphenyl ethers and their capacity to induce CYP1A by the Ah receptor mediated pathway. Chen, G., Konstantinov, A.D., Chittim, B.G., Joyce, E.M., Bols, N.C., Bunce, N.J. Environ. Sci. Technol. (2001) [Pubmed]
  7. Unexpected diversity of aryl hydrocarbon receptors in non-mammalian vertebrates: insights from comparative genomics. Hahn, M.E., Karchner, S.I., Evans, B.R., Franks, D.G., Merson, R.R., Lapseritis, J.M. J. Exp. Zoolog. Part A Comp. Exp. Biol. (2006) [Pubmed]
  8. 2,3,7,8-tetrachlorodibenzo-p-dioxin increases cardiac myocyte intracellular calcium and progressively impairs ventricular contractile responses to isoproterenol and to calcium in chick embryo hearts. Canga, L., Paroli, L., Blanck, T.J., Silver, R.B., Rifkind, A.B. Mol. Pharmacol. (1993) [Pubmed]
  9. Lethality and EROD-inducing potency of chlorinated chrysene in chick embryos. Gustafsson, E., Brunström, B., Nilsson, U. Chemosphere (1994) [Pubmed]
  10. Towards molecular understanding of species differences in dioxin sensitivity: initial characterization of Ah receptor cDNAs in birds and an amphibian. Karchner, S.I., Kennedy, S.W., Trudeau, S., Hahn, M.E. Mar. Environ. Res. (2000) [Pubmed]
  11. Induction of ethoxyresorufin O-deethylase (EROD) and endothelial activation of the heterocyclic amine Trp-P-1 in bird embryo hearts. Annas, A., Brunström, B., Brandt, I., Brittebo, E.B. Arch. Toxicol. (1998) [Pubmed]
  12. 2,3,7,8-Tetrachlorodibenzo-p-dioxin elicits aryl hydrocarbon receptor-mediated apoptosis in the avian DT40 pre-B-cell line through activation of caspases 9 and 3. Puebla-Osorio, N., Ramos, K.S., Falahatpisheh, M.H., Smith, R., Berghman, L.R. Comp. Biochem. Physiol. C Toxicol. Pharmacol. (2004) [Pubmed]
  13. Identification of CYP1A5 as the CYP1A enzyme mainly responsible for uroporphyrinogen oxidation induced by AH receptor ligands in chicken liver and kidney. Sinclair, P.R., Gorman, N., Walton, H.S., Sinclair, J.F., Lee, C.A., Rifkind, A.B. Drug Metab. Dispos. (1997) [Pubmed]
  14. Comparison of Ah receptor-mediated luciferase and ethoxyresorufin-O-deethylase induction in H4IIE cells: implications for their use as bioanalytical tools for the detection of polyhalogenated aromatic hydrocarbons. Sanderson, J.T., Aarts, J.M., Brouwer, A., Froese, K.L., Denison, M.S., Giesy, J.P. Toxicol. Appl. Pharmacol. (1996) [Pubmed]
  15. Effects of the TCDD congeners 3,3',4,4'-tetrachlorobiphenyl and 3,3',4,4'-tetrachloroazoxybenzene on lymphoid development in the bursa of Fabricius of the chick embryo. Nikolaidis, E., Brunström, B., Dencker, L. Toxicol. Appl. Pharmacol. (1988) [Pubmed]
  16. Hepatic microsomal ethoxyresorufin O-deethylase-inducing potency in ovo and cytosolic Ah receptor binding affinity of 2,3,7,8-tetrachlorodibenzo-p-dioxin: comparison of four avian species. Sanderson, J.T., Bellward, G.D. Toxicol. Appl. Pharmacol. (1995) [Pubmed]
  17. Variation in the molecular mass of the Ah receptor among vertebrate species and strains of rats. Poland, A., Glover, E. Biochem. Biophys. Res. Commun. (1987) [Pubmed]
  18. Characterization of cardiotoxicity induced by 2,3,7, 8-tetrachlorodibenzo-p-dioxin and related chemicals during early chick embryo development. Walker, M.K., Catron, T.F. Toxicol. Appl. Pharmacol. (2000) [Pubmed]
  19. Developmental regulation of the 3-methylcholanthrene- and dioxin-inducible CYP1A5 gene in chick embryo liver in vivo. Bentivegna, C.S., Ihnat, M.A., Baptiste, N.S., Hamilton, J.W. Toxicol. Appl. Pharmacol. (1998) [Pubmed]
  20. Fate of Ah-receptor agonists in organic household waste during anaerobic degradation--estimation of levels using EROD induction in organ cultures of chick embryo livers. Engwall, M., Schnürer, A. Sci. Total Environ. (2002) [Pubmed]
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