| Vitamin D(3) signalling to mast cells: A new regulatory axis. | |
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MedLine Citation:
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PMID: 20974277 Owner: NLM Status: In-Process |
Abstract/OtherAbstract:
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Excessive sun exposure or high acute doses of ultraviolet (UV)-B radiation promote cutaneous inflammation and genetic mutations, both of which can ultimately contribute to skin carcinogenesis. A major mediator synthesized in the epidermis in response to UVB irradiation is the secosteroid hormone vitamin D(3), and as such, considerable attention is now turning to the many physiologic processes that it regulates. Recent studies have uncovered an immunoregulatory interaction between vitamin D(3) and dermal mast cells for optimal protection against pathogenic outcomes associated with chronic UVB irradiation of the skin. Most biological effects of vitamin D(3), such as the regulation of transcription in target genes, occur when it binds to its nuclear receptor; however, some actions can also occur via a non-genomic signalling pathway. This review will focus on the relative importance of both pathways in the regulation of vitamin D(3)-mediated UVB protection and will highlight exciting recent findings that point to new research directions. |
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Authors:
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Chunping Yu; Boris Fedoric; Paul H Anderson; Angel F Lopez; Michele A Grimbaldeston |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-10-23 |
Journal Detail:
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Title: The international journal of biochemistry & cell biology Volume: 43 ISSN: 1878-5875 ISO Abbreviation: Int. J. Biochem. Cell Biol. Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2010-12-20 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9508482 Medline TA: Int J Biochem Cell Biol Country: Netherlands |
Other Details:
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Languages: eng Pagination: 41-6 Citation Subset: IM |
Copyright Information:
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Crown Copyright © 2010. Published by Elsevier Ltd. All rights reserved. |
Affiliation:
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Division of Human Immunology, Centre for Cancer Biology, SA Pathology, Adelaide 5000, South Australia, Australia. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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