Cutaneous pharmacologic cAMP induction induces melanization of the skin and improves recovery from ultraviolet injury in melanocortin 1 receptor‐intact or heterozygous skin-Reference-Cited by-同舟云学术

Cutaneous pharmacologic cAMP induction induces melanization of the skin and improves recovery from ultraviolet injury in melanocortin 1 receptor‐intact or heterozygous skin

Published:2019-08-24 Issue:1 Volume:33 Page:30-40
ISSN:1755-1471
Container-title:Pigment Cell & Melanoma Research
language:en
Short-container-title:Pigment Cell Melanoma Res

Author:

Bautista Robert‐Marlo¹²,Carter Katharine Marie¹,Jarrett Stuart Gordon¹³,Napier Dana¹,Wakamatsu Kazumasa⁴^ORCID,Ito Shosuke⁴^ORCID,D'Orazio John August¹³⁵^ORCID

Affiliation:

1. The Markey Cancer Center University of Kentucky Lexington KY USA

2. The Department of Surgery University of Kentucky Lexington KY USA

3. The Department of Toxicology and Cancer Biology University of Kentucky Lexington KY USA

4. The Fujita Health University Nagoya Aichi Japan

5. The Department of Pediatrics University of Kentucky Lexington KY USA

Funder

National University Cancer Institute, Singapore

Melanoma Research Alliance

National Institute of Environmental Health Sciences

Publisher

Wiley

Subject

Dermatology,General Biochemistry, Genetics and Molecular Biology,Oncology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1111/pcmr.12817

Reference46 articles.

1. α-MSH tripeptide analogs activate the melanocortin 1 receptor and reduce UV-induced DNA damage in human melanocytes

2. Modulation of forskolin-mediated adenylyl cyclase activation by constitutively active Gs -coupled receptors

3. Pharmacologic induction of epidermal melanin and protection against sunburn in a humanized mouse model;Amaro‐Ortiz A.;Journal of Visualized Experiments,2013

4. Receptor function, dominant negative activity and phenotype correlations for MC1R variant alleles

5. cAMP-independent non-pigmentary actions of variant melanocortin 1 receptor: AKT-mediated activation of protective responses to oxidative DNA damage

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