The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
The Aryl Hydrocarbon Receptor Mediates UVB Radiation–Induced Skin Tanning
Open accessAbstract
Melanogenesis is the vital response to protect skin cells against UVB-induced DNA damage. Melanin is produced by melanocytes, which transfer it to surrounding keratinocytes. Recently, we have shown that the aryl hydrocarbon receptor (AhR) is part of the UVB-stress response in epidermal keratinocytes. UVB triggers AhR signaling by generating the AhR ligand 6-formylindolo(3,2-b)carbazole from tryptophan. We show here that normal murine melanocytes express functional AhR. Using standard UVB tanning protocols, AhR-deficient mice were shown to tan significantly weaker than wild-type mice; in these mice, tyrosinase activity in the epidermis was lower as well. Tanning responses and tyrosinase activity, however, were normal in keratinocyte-specific conditional AhR knockout mice, indicating that release of melanogenic keratinocyte factors is unaffected by the UVB-AhR signaling pathway and that the diminished tanning response in AhR(-/-) mice is confined to the level of melanocytes. Accordingly, the number of dihydroxyphenylalanin-positive melanocytes increased significantly less on UVB irradiation in AhR(-/-) mice than in wild-type mice. This difference in melanocyte number was associated with a significantly reduced expression of stem cell factor-1 and c-kit in melanocytes of AhR(-/-) mice. Thus, the environmental signal sensor AhR links solar UVB radiation to skin pigmentation.
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“PAHs are potent activators of the aryl hydrocarbon receptor (AhR), which is a ligand-dependent transcription factor expressed in keratinocytes and melanocytes (Fritsche et al. 2007; Jux et al. 2011).”
From Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis (2018) · cites this paper as Jux et al. 2011
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Self-citation
Metadata
- Authors
- Jux, B., Kadow, S., Luecke, S., Rannug, A., Krutmann, J., & Esser, C.
- Affiliations
- Leibniz Institute of Environmental Medicine (DE)
- Karolinska Institutet (SE)
- Corresponding author
- Esser, Charlotte
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2011-01
- Volume
- 131
- Issue
- 1
- Pages
- 203-210
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W1966603244
- Cited by
- 156
- References
- 38
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 3 · 2023: 9 · 2022: 7 · 2021: 7 · 2020: 12 · 2019: 10 · 2018: 12 · 2017: 9 · 2016: 12 · 2015: 11 · 2014: 9 · 2013: 10 · 2012: 12
- FWCI
- 5.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › melanin and skin pigmentation
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Keywords
- aryl hydrocarbon receptor, UV-B radiation, tanning, melanogenesis, melanocytes, keratinocytes, FICZ, tryptophan metabolism, tyrosinase activity, CD117, melanocyte proliferation, skin pigmentation, conditional knockout mice
- MeSH terms
- Epidermal Cells, Animals, Cell Count, Cell Differentiation, Cells, Cultured, Epidermis, Melanins, Melanocytes, Mice, Inbred C57BL, Skin Pigmentation, Ultraviolet Rays, Keratinocytes, Receptors, Aryl Hydrocarbon, Mice, Knockout, Mice
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