Research paperProlonged depletion of AH receptor without alteration of receptor mRNA levels after treatment of cells in culture with 2,3,7,8-tetrachlorodibenzo-p-dioxin☆,☆☆
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2021, Molecular MetabolismCitation Excerpt :Immunoblot analysis also showed that Pygl protein expression was increased by the same concentrations of 3-MC (Figure 3B). Previous studies have shown that aryl hydrocarbon receptor (Ahr) protein is rapidly degraded when it binds ligands, such as 3-MC, via the ubiquitin-proteasome pathway [32–34]. The present results, showing that Ahr protein expression is dose-dependently reduced by 3-MC, are consistent with the previous findings (Figure 3B).
Benzo[a]pyrene and 2,3-benzofuran induce divergent temporal patterns of AhR-regulated responses in zebrafish embryos (Danio rerio)
2019, Ecotoxicology and Environmental SafetyAhR signaling pathways and regulatory functions
2018, Biochimie OpenHalowax 1051 affects steroidogenesis by down-regulation of aryl hydrocarbon and estrogen receptors and up-regulation of androgen receptor in porcine ovarian follicles
2016, ChemosphereCitation Excerpt :These results are not in full agreement with a study by Aluru et al. (2005) in which an increase in protein expression of AHR was found to be influenced by another AHR ligand, β-naphthoflavone, in rainbow trout hepatocytes; this could suggest ligand-dependent activity. Also, some data point out that the decrease of AHR protein expression is connected with degradation of the receptor following ligand binding rather than due to a decrease in AHR mRNA (Giannone et al., 1998; Pollenz, 2002), while our data also show a decrease in AHR mRNA. This suggests that polychlorinated naphathalenes act on both AHR gene and protein expression and are in agreement with the statement that most receptor agonists cause down-regulation (degradation) of their receptors.
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A preliminary report of portions of this research was presented at the 8th International Conference on Cytochrome P450, Lisbon, Portugal, 1994.
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This work was supported by a grant to A.B.O. from the Medical Research Council of Canada and grant CA28868 from the National Cancer Institute, U.S.A. to O. Hankinson (in whose laboratory part of the work of this study was performed by M.P.).
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M.P. was supported by a fellowship from the Swiss National Science Foundation.