Journal
PIGMENT CELL & MELANOMA RESEARCH
Volume 25, Issue 3, Pages 370-374Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1755-148X.2012.00990.x
Keywords
cAMP; HBD3; MAPK; MC1R; NDP-MSH; pigmentation
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Funding
- NHMRC [APP1023884]
- ARC of Australia [ARC-DP0771169]
- National Institutes of Health [NIH-R01DK064265]
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Binding of melanocortin peptide agonists to the melanocortin-1 receptor of melanocytes results in eumelanin production, whereas binding of the agouti signalling protein inverse agonist results in pheomelanin synthesis. Recently, a novel melanocortin-1 receptor ligand was reported. A beta-defensin gene mutation was found to be responsible for black coat colour in domestic dogs. Notably, the human equivalent, beta-defensin 3, was found to bind with high affinity to the melanocortin-1 receptor; however, the action of beta-defensin as an agonist or antagonist was unknown. Here, we use in vitro assays to show that beta-defensin 3 is able to act as a weak partial agonist for cAMP signalling in human embryonic kidney (HEK) cells expressing human melanocortin-1 receptor. beta-defensin 3 is also able to activate MAPK signalling in HEK cells stably expressing either wild type or variant melanocortin-1 receptors. We suggest that beta-defensin 3 may be a novel melanocortin-1 receptor agonist involved in regulating melanocyte responses in humans.
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