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Lightening up the UV response by identification of the arylhydrocarbon receptor as a cytoplasmatic target for ultraviolet B radiation
Jason E. Cline*,
Josef Abel*, and
*Institut für Umweltmedizinische Forschung (IUF), Auf'm Hennekamp 50, 40225 Düsseldorf, Germany; Chemical and Veterinary Control Laboratory, Josef-König-Strasse 40, 48147 Münster, Germany; Department of Pediatric Oncology, Hematology, and Immunology, Children's Hospital, Heinrich Heine University Medical Center, Moorenstrasse 5, 40225 Düsseldorf, Germany; ¶Institute of Environmental Medicine, Karolinska Institutet, Box 210, S-171 77 Stockholm, Sweden; and Institute for Biochemistry und Molecular Biology I, Heinrich Heine University, Universitätsstrasse 1, 40225 Düsseldorf, Germany
Communicated by Richard B. Setlow, Brookhaven National Laboratory, Upton, NY, March 19, 2007
Received for publication November 9, 2006.
UVB radiation-induced signaling in mammalian cells involvestwo major pathways: one that is initiated through the generationof DNA photoproducts in the nucleus and a second one that occursindependently of DNA damage and is characterized by cell surfacereceptor activation. The chromophore for the latter one hasbeen unknown. Here, we report that the UVB response involvestryptophan as a chromophore. We show that through the intracellulargeneration of photoproducts, such as the arylhydrocarbon receptor(AhR) ligand 6-formylindolo[3,2-b]carbazole, signaling eventsare initiated, which are transferred to the nucleus and thecell membrane via activation of the cytoplasmatic AhR. Specifically,AhR activation by UVB leads to (i) transcriptional inductionof cytochrome P450 1A1 and (ii) EGF receptor internalizationwith activation of the EGF receptor downstream target ERK1/2and subsequent induction of cyclooxygenase-2. The role of theAhR in the UVB stress response was confirmed in vivo by studiesemploying AhR KO mice.
Author contributions: J.A. and J.K. contributed equally to thiswork; E.F., A.R., P.F., J.A., and J.K. designed research; E.F.,C.S., C.C., T. Bernsmann, T. Bernshausen, M.W., U.H., J.E.C.,H. Hajimiragha, and P.S. performed research; L.-O.K. and H.Hanenberg contributed new reagents/analytic tools; E.F., T.Bernsmann, and P.F. analyzed data; and E.F., A.R., J.A., andJ.K. wrote the paper.
UVR Exposure Sensitizes Keratinocytes to DNA Adduct Formation.
S. Nair, V. D. Kekatpure, B. L. Judson, A. B. Rifkind, R. D. Granstein, J. O. Boyle, K. Subbaramaiah, J. B. Guttenplan, and A. J. Dannenberg (2009)
Cancer Prevention Research
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ROOT UV-B SENSITIVE2 Acts with ROOT UV-B SENSITIVE1 in a Root Ultraviolet B-Sensing Pathway.
C. D. Leasure, H. Tong, G. Yuen, X. Hou, X. Sun, and Z.-H. He (2009)
|Abstract »|Full Text »|PDF »
Langerhans Cell Maturation and Contact Hypersensitivity Are Impaired in Aryl Hydrocarbon Receptor-Null Mice.