111 citations
,
April 2006 in “Annals of the New York Academy of Sciences” This study found that preventing abnormal mineral ion homeostasis in vitamin D receptor knockout mice stopped bone abnormalities, while the animal's skin phenotype arose from direct receptor effects independent of vitamin D.
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.
140 citations
,
April 2004 in “The journal of investigative dermatology/Journal of investigative dermatology” This study found that mice lacking the 1αOHase enzyme, which is responsible for producing a key vitamin D metabolite, showed impaired epidermal differentiation and delayed recovery of skin barrier function after disruption.
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.
119 citations
,
October 1998 in “Endocrinology” This study found that normalizing mineral ion levels in vitamin D receptor-ablated mice prevented hyperparathyroidism, rickets, and osteomalacia, but alopecia persisted, indicating a separate role for the receptor in hair growth.
110 citations
,
November 1984 in “The American Journal of Medicine” This study observed that children with a genetically transmitted defect in the 1,25-dihydroxyvitamin D3 receptor experienced spontaneous healing of rickets as they aged, despite persistent mineral imbalances during treatment.
88 citations
,
October 1983 in “The Journal of clinical endocrinology and metabolism/Journal of clinical endocrinology & metabolism” In this study, distinct clinical responses and long-term resistances were observed in two pediatric patients with vitamin D-dependency type II, associated with abnormalities in their skin fibroblast interactions with 1,25-(OH)2D3.