53 citations
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May 2010 in “Journal of Cellular Physiology” This study found that mice lacking the Vitamin D receptor showed disrupted hair follicle cycling, which was partially restored with hedgehog signaling pathway activation, suggesting a role for this pathway in follicle regulation independent of vitamin D.
148 citations
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May 2008 in “The journal of investigative dermatology/Journal of investigative dermatology” This study found that mice lacking the vitamin D receptor (VDR) developed skin tumors more rapidly than those with normal VDR activity, regardless of 1,25-dihydroxyvitamin D(3) presence.
427 citations
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April 2008 in “Nature Protocols” 127 citations
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January 2008 in “PloS one” This study observed that the vitamin D receptor is crucial for hair follicle formation and altering tumor development in the Wnt signaling pathway, suggesting therapeutic potential for vitamin D analogues in related tumors.
81 citations
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January 2006 in “Journal of cellular physiology” This study found that the absence of the vitamin D receptor disrupts hair follicle structure during the first catagen in mice, linked to increased expression of the hairless gene.
92 citations
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May 2004 in “Journal of Investigative Dermatology” 180 citations
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January 2002 in “The journal of investigative dermatology/Journal of investigative dermatology” This study observed that vitamin D receptor knockout mice exhibit impaired epidermal differentiation and progressive hair loss, suggesting the importance of the vitamin D receptor in normal skin and hair follicle development.
380 citations
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March 2000 in “Proceedings of the National Academy of Sciences” This study demonstrates that mice with ectopic expression of the human GLI-1 gene in their skin developed tumors resembling human basal cell carcinoma, suggesting that GLI-1 is central to tumor development without additional p53 or Ha ras mutations.
333 citations
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March 2000 in “Proceedings of the National Academy of Sciences” In this study, researchers established that increased expression of the human GLI-1 gene in mouse skin leads to the development of tumors that closely resemble human basal cell carcinomas, without requiring additional mutations in the p53 or Ha ras genes.