ArticleExperimental dermatology2013
Functional melanocortin 1 receptor Mc1r is not necessary for an inflammatory response to UV radiation in adult mouse skin.
Article in Experimental dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Implication of Immunobiological Function of Melanocytes in Dermatology.Clinical reviews in allergy & immunology · 2025Review
- Replacement of Arg with Nle and modified D-Phe in the core sequence of MSHs, Ac-His-D-Phe-Arg-Trp-NHEuropean journal of medicinal chemistry · 2018Article
- Design of MC1R Selective γ-MSH Analogues with Canonical Amino Acids Leads to Potency and Pigmentation.Journal of medicinal chemistry · 2017Article
- A melanin-independent interaction between Mc1r and Met signaling pathways is required for HGF-dependent melanoma.International journal of cancer · 2015Article
- Is Mc1r an important regulator of non-pigmentary responses to UV radiation?Experimental dermatology · 2013Article
- Article
- HGF/SF increases number of skin melanocytes but does not alter quality or quantity of follicular melanogenesis.PloS one · 2013Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
The G-protein-coupled receptor, Mc1r, plays a major role in pigment production and has been reported to be important in the inflammatory response. We have investigated the effect of deficiency in Mc1r on UV-induced inflammation. Mice on the same genetic background were used - C57BL/6-c (albino), C57BL/6 (black), C57BL/6-Mc1r(e/e) deficient (yellow). FACS analysis of disaggregated skin showed a similar dose-dependent increase in Ly6G(+) and CD11b(+) cells in response to UV radiation in all groups. No differences in UV-induced edema or in DNA damage were detected between groups. The contact hypersensitivity response, neonatal immune tolerance and UV immunosuppression were all similar in C57BL/6 and C57BL/6-Mc1r(e/e) mice. We conclude that the absence of Mc1r does not impair the inflammatory response to UV radiation or the generation of immunosuppression.
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Registered trials
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