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This study found that in a mouse model with hereditary 1,25-dihydroxyvitamin D resistant rickets, a mutant vitamin D receptor lacking hormone-binding ability could restore normal hair cycling and affect parathyroid hormone regulation.

This study reported a case of hereditary vitamin D–resistant rickets caused by a single heterozygous missense mutation in the VDR gene, showing dominant-negative effects and reduced response to 1,25-dihydroxyvitamin D3.

This study discovered a novel interaction between the vitamin D receptor and LEF1, essential for normal Wnt signaling in keratinocytes, which is crucial for regular hair cycling.

This review discusses the association between vitamin D receptor polymorphisms and polycystic ovary syndrome, noting the need for further research on their impact on the disorder's manifestations.

This study identified a novel nonsense mutation in the VDR gene in two patients with hereditary vitamin D resistant rickets and alopecia, leading to resistance to 1,25-dihydroxyvitamin D3.

This study found that vitamin D receptor activation in primary keratinocytes can occur independently of the 1,25-dihydroxyvitamin D₃ ligand, likely through interaction with retinoid X receptors.

Lack of small, fine hair on the front hairline is a key sign of frontal fibrosing alopecia.

In this study, VD(3) pretreatment increased hair follicle formation in a rat model by promoting dermal papilla cell differentiation, suggesting potential for hair regeneration therapy.

This study identified the Hairless (Hr) gene-encoded protein as a corepressor that plays a crucial role in maintaining skin and hair by regulating epithelial stem cell differentiation and gene expression via chromatin remodeling, which may impact both development and disease.

This study found that vitamin D deficiency in patients with alopecia areata was associated with greater disease severity and longer duration, but not with disease pattern or vitamin D receptor expression.

In this study, researchers observed that the absence of a functional vitamin D receptor in mice leads to impaired hair follicle regeneration due to defects in keratinocyte stem cells, resulting in alopecia.

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.

In this study, the researchers found that vitamin D and calcium signaling in keratinocytes are essential for normal skin regeneration after wounding, with deficiencies significantly delaying wound closure and re-epithelialization in mice.

This study found that the protein hairless acts as both a corepressor and coactivator of the vitamin D receptor, influencing gene transcription in a ligand-selective manner.

This study created a humanized mouse model of hereditary vitamin D-resistant rickets that lacks alopecia, indicating the mutant receptor's potential to explore the syndrome's characteristics beyond vitamin D binding.

This study suggests that while VDR is crucial for maintaining hair follicles in mice, their degeneration may be linked to impaired cell migration during hair growth phases rather than stem cell loss.

In this study, mutations in the vitamin D receptor were identified in Brazilian children with rickets and alopecia, leading to impaired receptor activation and reduced 24-hydroxylase expression.

This article reviews the multifaceted roles of vitamin D beyond bone health and notes its potential involvement in reducing risks of certain cancers and autoimmune diseases, but it presents no new clinical results.

This study suggests that impaired VDR signaling in mice leads to dysregulated Ddit4 expression, impacting hair cycle progression and wound healing.

This study concluded that the hairless protein interacts with the vitamin D receptor to repress transcription crucial for hair cycling, employing multiple protein interfaces and modulating chromatin structure.

This chapter discusses the molecular biology of the vitamin D receptor in gene transcription and reports no new results; it highlights recent findings on receptor activity independent of its usual ligand.

This study observed a potential relationship between the canonical Wnt signalling pathway and the expression of the vitamin D receptor in alopecia, suggesting a link worth further exploration.

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.

This study found that a novel missense mutation in the vitamin D receptor caused hereditary 1,25-dihydroxyvitamin D-resistant rickets with alopecia by disrupting protein function, highlighting the importance of DNA binding in hair development.

This study suggests that lower serum and tissue vitamin D receptor levels in alopecia areata and androgenetic alopecia patients may play a role in the pathogenesis of these hair diseases.

This study found that treatment with vitamin D increased the expression of LL-37 through the vitamin D receptor in cultured sebocytes.

This research suggests that the vitamin D receptor may regulate hair follicle cycling and provide genoprotection against skin carcinogenesis through a mechanism independent of 1,25-dihydroxyvitamin D3, based on evidence from mouse models.

A genetic mutation caused severe rickets and alopecia in an Indian patient, but high-dose calcium and phosphate treatment improved their condition.

This study demonstrated that both HR isoforms are expressed in keratinocytes, but HRDelta1072-1126 lacks corepressor activity and may act as a coactivator by inhibiting HDAC recruitment to the VDR transcriptional complex.

This study suggests that vitamin D-upregulated protein 1 (VDUP1) might play a unique role in regulating the differentiation of epidermal cells.