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Blockade by SB203580 of Cyp1a1 Induction by 2,3,7,8-Tetrachlorodibenzo-p-dioxin, and the Possible Mechanism: Possible Involvement of the p38 Mitogen-Activated Protein Kinase Pathway in Shuttling of Ah Receptor Overexpressed in COS-7 Cells
Department of Molecular Genetics, Institute of Development, Aging, and Cancer, Tohoku University, Sendai 980-8575, Japan
aAddress for correspondence: Hideaki Kikuchi Ph.D., Professor, Division of Cell Technology, Department of Biochemistry and Biotechnology, Faculty of Agriculture and Life Science, Hirosaki University, 3-Bunkyo-cho, Hirosaki 036-8561, Japan. Voice/fax: +81-172-39-3586. e-mail: hkikuchi{at}cc.hirosaki-u.ac.jp *Current address: Mitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida, Tokyo 194-8511, Japan.
A transiently overexpressed aryl hydrocarbon receptor (AhR) became translocated into the nucleus of COS-7 cells without treatment with any ligand, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin. This spontaneous AhR translocation into the nucleus was reduced by pretreatment of the recipient cells with the p38 mitogen-activated protein (MAP) kinase inhibitor SB203580
Key Words: Ah receptor • SB203580 • p38 MAP kinase • Cyp1a1 • dioxin
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