NDLI: UVB-induced association of tumor necrosis factor (TNF) receptor 1/TNF receptor-associated factor-2 mediates activation of Rel proteins.

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UVB-induced association of tumor necrosis factor (TNF) receptor 1/TNF receptor-associated factor-2 mediates activation of Rel proteins.

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UVB-induced association of tumor necrosis factor (TNF) receptor 1/TNF receptor-associated factor-2 mediates activation of Rel proteins.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Van Hogerlinden, M. Toftgård, R. Tobin, D.
Description	Author Affiliation: Tobin D ( Department of Bioscience at Novum, Karolinska Institute, NOVUM, Huddinge, Sweden.);
Abstract	Exposure of mammalian skin to UV light results in induced gene transcription, playing a role in inflammation, immunosuppression, and tumor promotion. One important group of transcription factors induced by UV radiation is composed of members of the Rel/NF-kappa B family, which are known to play a major role in the transcriptional activation of many genes encoding inflammatory cytokines, adhesion molecules, and viral proteins. However, the upstream events in the transduction of the UVB signal to Rel protein activity are, as yet, unknown. Here, we provide biochemical evidence that exposure of keratinocytes to UVB causes rapid association of tumor necrosis factor (TNF) receptor 1 with its downstream partner TRAF-2. The functional relevance of this association is demonstrated by experiments showing that expression of a dominant negative TNF receptor 1 or TRAF-2 protein inhibits UVB-induced Rel-dependent transcription. Inclusion of a neutralizing antibody toward TNF alpha has no effect on UVB activation of a Rel-responsive reporter gene. Therefore, UVB-induced activation of Rel proteins via TNF receptor 1, independent of ligand activation, is a key component in the UV response in keratinocytes.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	2
Volume Number	95
Language	English
Publisher	National Academy of Sciences
Publisher Date	1998-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Keratinocytes Metabolism Radiation Effects NF-kappa B Oncogenes Proteins Receptors, Tumor Necrosis Factor Animals Cell Line Gene Expression Regulation Mice Genetics Signal Transduction TNF Receptor-Associated Factor 2 Ultraviolet Rays Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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