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Skin abnormalities generated by temporally controlled RXRα mutations in mouse epidermis

Nuclear receptors for retinoids (RARs) and vitamin D (VDR), and for some other ligands (TRs, PPARs and LXRs), may be critical in the development and homeostasis of mammalian epidermis1, 2, 3, 4, 5, 6, 7, 8. It is believed that these receptors form heterodimers with retinoid X receptors (RXRs) to act... Full description

Journal Title: Nature 2000, Vol.407(6804), p.633
Main Author: Mei Li
Other Authors: Arup Kumar Indra , Xavier Warot , Jacques Brocard , Nadia Messaddeq , Shigeaki Kato , Daniel Metzger , Pierre Chambon
Format: Electronic Article Electronic Article
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ID: ISSN: 0028-0836 ; E-ISSN: 1476-4687 ; DOI: 10.1038/35036595
Link: http://dx.doi.org/10.1038/35036595
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recordid: nature_a10.1038/35036595
title: Skin abnormalities generated by temporally controlled RXRα mutations in mouse epidermis
format: Article
creator:
  • Mei Li
  • Arup Kumar Indra
  • Xavier Warot
  • Jacques Brocard
  • Nadia Messaddeq
  • Shigeaki Kato
  • Daniel Metzger
  • Pierre Chambon
subjects:
  • Sciences (General)
  • Physics
ispartof: Nature, 2000, Vol.407(6804), p.633
description: Nuclear receptors for retinoids (RARs) and vitamin D (VDR), and for some other ligands (TRs, PPARs and LXRs), may be critical in the development and homeostasis of mammalian epidermis1, 2, 3, 4, 5, 6, 7, 8. It is believed that these receptors form heterodimers with retinoid X receptors (RXRs) to act as transcriptional regulators9, 10. However, most genetic approaches aimed at establishing their physiological functions in the skin have been inconclusive owing either to pleiotropic effects and redundancies between receptor isotypes in gene knockouts, or to equivocal interpretation of dominant-negative mutant studies in transgenic mice1, 13, 14, 15. Moreover, knockout of RXR, the main skin RXR isotype, is lethal in utero before skin formation11, 12, 16, 17. Here we have resolved these problems by developing an efficient technique to create spatio-temporally controlled somatic mutations in the mouse. We used tamoxifen-inducible Cre–ER T recombinases18, 19 to ablate RXR selectively in adult mouse keratinocytes. We show that RXR has key roles in hair cycling, probably through RXR/VDR heterodimers, and in epidermal keratinocyte proliferation and differentiation.
language:
source:
identifier: ISSN: 0028-0836 ; E-ISSN: 1476-4687 ; DOI: 10.1038/35036595
fulltext: fulltext
issn:
  • 0028-0836
  • 00280836
  • 1476-4687
  • 14764687
url: Link


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titleSkin abnormalities generated by temporally controlled RXRα mutations in mouse epidermis
creatorMei Li ; Arup Kumar Indra ; Xavier Warot ; Jacques Brocard ; Nadia Messaddeq ; Shigeaki Kato ; Daniel Metzger ; Pierre Chambon
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descriptionNuclear receptors for retinoids (RARs) and vitamin D (VDR), and for some other ligands (TRs, PPARs and LXRs), may be critical in the development and homeostasis of mammalian epidermis1, 2, 3, 4, 5, 6, 7, 8. It is believed that these receptors form heterodimers with retinoid X receptors (RXRs) to act as transcriptional regulators9, 10. However, most genetic approaches aimed at establishing their physiological functions in the skin have been inconclusive owing either to pleiotropic effects and redundancies between receptor isotypes in gene knockouts, or to equivocal interpretation of dominant-negative mutant studies in transgenic mice1, 13, 14, 15. Moreover, knockout of RXR, the main skin RXR isotype, is lethal in utero before skin formation11, 12, 16, 17. Here we have resolved these problems by developing an efficient technique to create spatio-temporally controlled somatic mutations in the mouse. We used tamoxifen-inducible Cre–ER T recombinases18, 19 to ablate RXR selectively in adult mouse keratinocytes. We show that RXR has key roles in hair cycling, probably through RXR/VDR heterodimers, and in epidermal keratinocyte proliferation and differentiation.
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