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.
109 citations
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October 2007 in “American Journal of Human Genetics” This study found that postnatal treatment with recombinant EDA normalized adult teeth, improved sweating, and restored normal lacrimation in dogs with XLHED, suggesting its potential as a treatment for the condition.
43 citations
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December 2006 in “The American journal of pathology” This study found that Edar signaling plays a role in regulating the hair cycle and apoptosis in hair follicle keratinocytes during the catagen phase in mice.
57 citations
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February 2006 in “Journal of Investigative Dermatology” Cylindromas likely originate from hair follicle stem cells, not sweat glands.
64 citations
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March 2005 in “Journal of Investigative Dermatology” This study found that brain-derived neurotrophic factor (BDNF) inhibited hair shaft elongation and induced premature catagen development in cultured human hair follicles, partially through transforming growth factor β2.
118 citations
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January 2004 in “European Journal of Cell Biology” Balanced protease activity is crucial for healthy skin and hair development.
122 citations
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June 2002 in “Genes & Development” This study found that K17 is crucial for the structural integrity and survival of hair-producing cells, with K17 null mice developing alopecia due to hair fragility and follicular alterations.
96 citations
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October 2000 in “The FASEB Journal” In this study, researchers found that p75 neurotrophin receptor signaling affects apoptosis during hair follicle regression in mice, and altering its activity might help manage disorders involving early catagen entry.
47 citations
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April 2000 in “The American journal of pathology” This study found that overexpressing human Bcl-2 in mice protected epidermal keratinocytes from UVB-induced apoptosis but unexpectedly increased apoptosis during hair follicle regression and chemotherapy.