MC1R and NR4A receptors in cellular stress and DNA repair: implications for UVR protection

Yin, Kelvin, Sturm, Richard A. and Smith, Aaron G. (2014) MC1R and NR4A receptors in cellular stress and DNA repair: implications for UVR protection. Experimental Dermatology, 23 7: 449-452. doi:10.1111/exd.12420


Author Yin, Kelvin
Sturm, Richard A.
Smith, Aaron G.
Title MC1R and NR4A receptors in cellular stress and DNA repair: implications for UVR protection
Journal name Experimental Dermatology   Check publisher's open access policy
ISSN 1600-0625
0906-6705
Publication date 2014
Year available 2014
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1111/exd.12420
Open Access Status
Volume 23
Issue 7
Start page 449
End page 452
Total pages 4
Place of publication Chichester, West Sussex, United Kingdom
Publisher Wiley-Blackwell
Collection year 2015
Language eng
Abstract Ultraviolet radiation (UVR) is the most common mutagen which melanocytes are exposed to. UVR causes a diverse range of DNA photolesions contributing to genome instability and promotes melanoma and non-melanoma development. Melanocytes are pigment-producing cells that synthesise the photoprotective melanins when the melanocortin-1-receptor (MC1R) is activated. MC1R is a G-protein-coupled receptor expressed predominantly in melanocytes. Its signalling pathway has been directly linked to melanogenesis, enhanced cytoprotection against UV damage and augmented DNA repair response. Interestingly, previous studies have revealed that MC1R signalling induces the transcription of the NR4A subfamily of orphan nuclear receptors in response to UV. In line with this, studies have also observed that NR4A receptors are recruited to distinct nuclear foci in response to cellular stress, independent of their transcriptional roles. Here we review the regulated expression of NR4A2 and its potential roles upon cellular stress conditions. Current work in developing synthetic NR4A2 agonists further provides exciting avenues for exploring the potential role of NR4A2 as an anti-skin cancer drug target.
Keyword DNA repair
MC1R
NR4A2
UVR
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Published online ahead of print 23 April 2014.

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Official 2015 Collection
School of Biomedical Sciences Publications
School of Medicine Publications
Institute for Molecular Bioscience - Publications
 
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Created: Thu, 22 May 2014, 10:36:15 EST by Susan Allen on behalf of Institute for Molecular Bioscience