UVB-induced association of tumor necrosis factor (TNF) receptor 1/TNF receptor-associated factor-2 mediates activation of Rel proteins
Open accessAbstract
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-κB 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 TNFα 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.
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TNFR is clustered and internalized in keratinocytes after UVB irradiation, coupled with recruitment of TRADD and TRAF-2, and there appears to be crosstalk between TNFR and FADD-induced apoptotic pathways.
“On the other hand, tumor necrosis factor receptor (TNFR) is clustered and internalized in keratinocytes after UVB irradiation. This process is coupled with the recruitment of TNFR1-associated death protein and TNFR-associated factor-2 (TRAF-2) in the human or murine keratinocyte cell lines, respectively. There appears to be crosstalk between TNFR and FADD-induced apoptotic pathways [36].”
From Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy (2013) · cites this paper as [36]
The results section reports that UVB irradiation causes TNFR1–TRAF-2 association in murine keratinocytes, with similar results in primary human keratinocytes. The Discussion describes TRADD as an indirect link between TNFR1 and TRAF-2 and proposes a balance between TRADD–FADD apoptotic signaling and TRADD–TRAF-2 protective signaling. Our copy does not report TNFR clustering or internalization, or directly demonstrate UVB-induced TRADD recruitment. Page numbers were not available in the indexed passages. (LLM, conf=0.86)
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- Authors
- Tobin, D., van Hogerlinden, M., & Toftgård, R.
- Affiliations
- Karolinska Institutet (SE)
- Department of Bioscience at Novum, Karolinska Institute, NOVUM, S-141 57, Huddinge, Sweden
- ORCID
- Tobin, Derek
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1998-01-20
- Volume
- 95
- Issue
- 2
- Pages
- 565-569
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC18460
- OpenAlex
- W2023735966
- Cited by
- 55
- References
- 3
- Citations by year
- 2026: 1 · 2022: 1 · 2021: 2 · 2020: 1 · 2018: 1 · 2017: 2 · 2015: 1 · 2014: 1 · 2013: 4 · 2012: 1
- FWCI
- 2.66
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- UV-B radiation, TNF receptor 1, TRAF2, keratinocytes, signal transduction, dominant negative receptor, skin inflammation
- MeSH terms
- Animals, Cell Line, Gene Expression Regulation, Oncogenes, Proteins, Ultraviolet Rays, Signal Transduction, Keratinocytes, NF-kappa B, Receptors, Tumor Necrosis Factor, TNF Receptor-Associated Factor 2, Mice
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