This Article Full Text Full Text (PDF) Supplemental Data Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Vogel, C. F. A. Articles by Matsumura, F. Search for Related Content PubMed PubMed Citation Articles by Vogel, C. F. A. Articles by Matsumura, F. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Compound via MeSH Substance via MeSH Hazardous Substances DB 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN

RelB, a New Partner of Aryl Hydrocarbon Receptor-Mediated Transcription

Department of Environmental Toxicology (C.F.A.V., E.S., W.L., P.W., F.M.), University of California, Davis, Davis, California 95616; and Institut National de la Santé et de la Recherche Médicale Unité 844 (G.L.), Molecular and Cellular Endocrinology of Cancers, Montpellier F-34295, France

Address all correspondence and requests for reprints to: Christoph F. A. Vogel, Department of Environmental Toxicology, University of California, Davis, One Shields Avenue, Davis, California 95616. E-mail: cfvogel{at}ucdavis.edu.

The nuclear factor-B (NF-B) transcription factor family has a crucial role in rapid responses to stress and pathogens. We show that the NF-B subunit RelB is functionally associated with the aryl hydrocarbon receptor (AhR) and mediates transcription of chemokines such as IL-8 via activation of AhR and protein kinase A. RelB physically interacts with AhR and binds to an unrecognized RelB/AhR responsive element of the IL-8 promoter linking two signaling pathways to activate gene transcription. We found a time-dependent recruitment of AhR to the RelB/AhR responsive element site of IL-8 mediated by the AhR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) and via activation of protein kinase A. Furthermore, NF-B-binding sites that are preferentially recognized by RelB/p52 are a target for RelB/AhR complexes without addition of any stimuli, implicating the endogenous function of the AhR. RelB/AhR complexes are also found to bind on xenobiotic responsive element, and RelB drastically increases the 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced xenobiotic responsive element reporter activity. The interaction of RelB with AhR signaling, and AhR with NF-B RelB signaling pathways represent a new mechanism of cross talk between the two transcription factors.

This article has been cited by other articles:

				A. Kimura, T. Naka, T. Nakahama, I. Chinen, K. Masuda, K. Nohara, Y. Fujii-Kuriyama, and T. Kishimoto Aryl hydrocarbon receptor in combination with Stat1 regulates LPS-induced inflammatory responses J. Exp. Med., August 31, 2009; 206(9): 2027 - 2035. [Abstract] [Full Text] [PDF]

				M. J. Jenny, S. I. Karchner, D. G. Franks, B. R. Woodin, J. J. Stegeman, and M. E. Hahn Distinct Roles of Two Zebrafish AHR Repressors (AHRRa and AHRRb) in Embryonic Development and Regulating the Response to 2,3,7,8-Tetrachlorodibenzo-p-dioxin Toxicol. Sci., August 1, 2009; 110(2): 426 - 441. [Abstract] [Full Text] [PDF]

				B. Jux, S. Kadow, and C. Esser Langerhans Cell Maturation and Contact Hypersensitivity Are Impaired in Aryl Hydrocarbon Receptor-Null Mice J. Immunol., June 1, 2009; 182(11): 6709 - 6717. [Abstract] [Full Text] [PDF]

				C. Demetriades and G. Mosialos The LMP1 Promoter Can Be Transactivated Directly by NF-{kappa}B J. Virol., May 15, 2009; 83(10): 5269 - 5277. [Abstract] [Full Text] [PDF]

				N. Ishimaru, A. Takagi, M. Kohashi, A. Yamada, R. Arakaki, J. Kanno, and Y. Hayashi Neonatal Exposure to Low-Dose 2,3,7,8-Tetrachlorodibenzo-p-Dioxin Causes Autoimmunity Due to the Disruption of T Cell Tolerance J. Immunol., May 15, 2009; 182(10): 6576 - 6586. [Abstract] [Full Text] [PDF]

				B. Dong and F. Matsumura The Conversion of Rapid TCCD Nongenomic Signals to Persistent Inflammatory Effects via Select Protein Kinases in MCF10A Cells Mol. Endocrinol., April 1, 2009; 23(4): 549 - 558. [Abstract] [Full Text] [PDF]

				P. van Baarlen, F. J. Troost, S. van Hemert, C. van der Meer, W. M. de Vos, P. J. de Groot, G. J. E. J. Hooiveld, R.-J. M. Brummer, and M. Kleerebezem Differential NF-{kappa}B pathways induction by Lactobacillus plantarum in the duodenum of healthy humans correlating with immune tolerance PNAS, February 17, 2009; 106(7): 2371 - 2376. [Abstract] [Full Text] [PDF]

				C. J. Baglole, S. B. Maggirwar, T. A. Gasiewicz, T. H. Thatcher, R. P. Phipps, and P. J. Sime The Aryl Hydrocarbon Receptor Attenuates Tobacco Smoke-induced Cyclooxygenase-2 and Prostaglandin Production in Lung Fibroblasts through Regulation of the NF-{kappa}B Family Member RelB J. Biol. Chem., October 24, 2008; 283(43): 28944 - 28957. [Abstract] [Full Text] [PDF]

				C. A. Leontiou, M. Gueorguiev, J. van der Spuy, R. Quinton, F. Lolli, S. Hassan, H. S. Chahal, S. C. Igreja, S. Jordan, J. Rowe, et al. The Role of the Aryl Hydrocarbon Receptor-Interacting Protein Gene in Familial and Sporadic Pituitary Adenomas J. Clin. Endocrinol. Metab., June 1, 2008; 93(6): 2390 - 2401. [Abstract] [Full Text] [PDF]

				A. J. Fusco, O. V. Savinova, R. Talwar, J. D. Kearns, A. Hoffmann, and G. Ghosh Stabilization of RelB Requires Multidomain Interactions with p100/p52 J. Biol. Chem., May 2, 2008; 283(18): 12324 - 12332. [Abstract] [Full Text] [PDF]