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dc.contributor.authorCottle, Denny
dc.contributor.authorKretzschmar, K
dc.contributor.authorGollnick, HP
dc.contributor.authorQuist, SR
dc.date.accessioned2015-07-15T10:43:16Z
dc.date.available2015-07-15T10:43:16Z
dc.date.issued2016-01
dc.identifier.citationCottle et al. British Journal of Dermatology (2015) Vol. 174, Issue 1, pp. 204-208. doi:10.1111/bjd.14048
dc.identifier.issn0007-0963
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/248966
dc.description.abstractBackground- The role of p53 in the pathogenesis of skin diseases such as plaque-type psoriasis has long been questioned but never resolved. Objectives- In this study we set out to determine the contribution of p53 activity to defective interfollicular epidermal skin differentiation in a murine hyperproliferative skin model. Methods- We used the tamoxifen-inducible K14MycER mouse model which exhibits abnormal epidermal differentiation in response to high MYC activity, crossed with p53 knock-out mice. Results- We show that genetic deletion of p53 leads to improvements in granular layer formation. Furthermore, we show that p53 activity regulates down-stream expression of Keratin 6a, Pparb/d and Pparg and is regulated upstream by retinoic acid signalling-dependent mechanisms. Conclusion- We conclude aberrant non-apoptotic p53 activity contributes, in-part, to abnormal differentiation and granular layer defects.
dc.description.sponsorshipThis work was supported by the Prof. Fiona M. Watt via the MRC, Wellcome Trust, CRUK, EU FP7 programme, the University of Cambridge, Hutchison Whampoa Ltd. This work was also supported by A/ Prof. Ian M. Smyth and Monash University.
dc.languageEnglish
dc.language.isoen
dc.publisherWiley
dc.rightsCreative Commons Attribution 4.0 International License
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectepidermis
dc.subjectskin
dc.subjectpsoriasis
dc.subjectparakeratosis
dc.subjectMYC
dc.subjectp53
dc.subjectkeratin 6
dc.subjectPPAR
dc.subjectinterfollicular epidermis
dc.subjectretinoic acid
dc.titlep53 activity contributes to defective interfollicular epidermal differentiation in hyperproliferative murine skin.
dc.typeArticle
dc.description.versionThis is the final version of the article. It first appeared from Wiley via http://dx.doi.org/10.1111/bjd.14048
prism.endingPage208
prism.publicationDate2015
prism.publicationNameBr J Dermatol
prism.startingPage204
prism.volume174
dc.rioxxterms.funderMRC
dc.rioxxterms.funderWellcome Trust
dc.rioxxterms.funderCRUK
rioxxterms.versionofrecord10.1111/bjd.14048
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2015-11-20
dc.identifier.eissn1365-2133
rioxxterms.typeJournal Article/Review
cam.issuedOnline2015-11-20


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Creative Commons Attribution 4.0 International License
Except where otherwise noted, this item's licence is described as Creative Commons Attribution 4.0 International License