1533 citations
,
October 2008 in “Endocrine reviews” This research highlights that engineered mice lacking the vitamin D receptor show multiple health issues similar to human vitamin D deficiency, underscoring the widespread impacts of the vitamin D endocrine system.
143 citations
,
May 2007 in “Proceedings of the National Academy of Sciences” This study found that absence of the vitamin D receptor in keratinocytes impairs canonical Wnt signaling and leads to alopecia due to defects in keratinocyte stem cells.
137 citations
,
September 2005 in “Proceedings of the National Academy of Sciences of the United States of America” In this study, researchers found that transgenic expression of the Hairless gene in keratinocytes can restore hair follicle regeneration in Hr-deficient mice by repressing Wise, a modulator of Wnt signaling.
144 citations
,
December 2004 in “Molecular Endocrinology” This study found that the effects of the vitamin D receptor on hair follicle cycling in mice are independent of its ability to bind a hormone, with specific domain mutations influencing hair regrowth outcomes.
335 citations
,
March 2004 in “Development” This study found that continuous β-catenin signaling in adult mouse epidermis can reprogram hair follicles to form benign tumors, which regress after the signaling is discontinued.
561 citations
,
April 2003 in “Journal of Investigative Dermatology” CD34 is a marker for isolating stem-like cells in mouse hair follicles.
277 citations
,
July 2002 in “Molecular Endocrinology” In this study, homozygous VDR null mutant mice exhibited nonfunctional vitamin D receptors, leading to growth abnormalities and revealing the limited physiological importance of vitamin D pathways outside the classical receptor.
297 citations
,
January 2002 in “Development” In this study, repressing β-catenin/Lef1 signalling in mouse epidermis led to progressive hair loss, dermal cysts, and spontaneous skin tumors with sebaceous differentiation, indicating altered keratinocyte differentiation and potential tumourigenic processes.
180 citations
,
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.
115 citations
,
December 2001 in “Endocrinology” This study found that restoring vitamin D receptor expression specifically in the keratinocytes of VDR null mice prevented alopecia and enhanced hair follicle response during anagen initiation.
21 citations
,
December 2001 in “Endocrinology” This study found that restoring vitamin D receptor expression in keratinocytes of VDR null mice prevents alopecia by enhancing the hair follicle's proliferative response during anagen initiation.
555 citations
,
July 2001 in “Genes & Development” This study found that Tcf3 and Lef1 differently regulate cell differentiation in multipotent skin stem cells, with Tcf3 promoting follicle-like features and Lef1, when modified, promoting sebocyte differentiation.
137 citations
,
April 2001 in “Journal of Clinical Investigation” This study found that alopecia in VDR-null mice persists despite undetectable vitamin D levels, indicating a defect in epithelial-mesenchymal communication due to the absence of ligand-independent receptor function.
303 citations
,
October 2000 in “Nature” This study found that RXRα plays a critical role in hair cycling and keratinocyte functions in mice, likely through its interaction with VDR in epidermal cells.
114 citations
,
June 2000 in “Endocrinology” In this study, the researchers found that alopecia in VDR null mice is likely due to issues with hair cycle initiation rather than defects in keratinocyte proliferation or differentiation.
29 citations
,
June 2000 in “Endocrinology” This study suggests that alopecia in vitamin D receptor null mice is due to impaired initiation of the hair cycle rather than defects in keratinocyte proliferation or differentiation.
