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This study observed that 25-hydroxyvitamin D3 restored rickets symptoms in genetically modified rats, suggesting its direct action through vitamin D receptor pathways.

In this study, only Vdr-knockout rats showed both abnormal skin formation and alopecia, which may provide insights into vitamin D receptor function and its role in the hair growth cycle.

This study describes a patient with hereditary vitamin D resistant rickets (HVDRR) who, despite having a truncated vitamin D receptor, did not exhibit typical hair or skin abnormalities, suggesting possible compensation via interactions with other proteins.

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.

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 study identified new dietary ligands for the human vitamin D receptor, including curcumin and gamma-tocotrienol, which may influence its biological functions.

This review discusses the molecular role of the vitamin D receptor in regulating various biological actions such as bone mineralization and reports no new clinical results, highlighting the complexity of vitamin D's function in multiple tissues.

This study found that the vitamin D receptor, but not its ligand, regulates genes involved in hair cycle progression, suggesting a role in integrating hormone signaling pathways for hair and epidermal functions.

This study found that lower expression of VDR protein in breast cancer patients is associated with increased bone metastasis and poorer prognosis, making it a significant prognostic factor.

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.

This study found that humanized mouse models expressing mutated or reduced levels of the vitamin D receptor were able to maintain normal mineral homeostasis and prevent typical symptoms of vitamin D resistance.

This case report documents a female toddler with novel compound heterozygous mutations in the VDR gene causing hereditary 1,25-dihydroxyvitamin D-resistant rickets, expanding the known mutation spectrum for this disease.

This review discusses the regulation and function of vitamin D and its receptor in skin cells, highlighting their roles in processes such as proliferation inhibition, differentiation, and innate immunity, but reports no new results.

This review examines the functions of vitamin D and its receptor in skin and explores how these are regulated, reporting no new clinical results.

This review examines the role of nuclear hormone receptors in skin wound repair processes and reports no new clinical results, highlighting the importance of their interaction with skin cells for effective healing.

This study found that the vitamin D receptor is crucial for initiating the postnatal hair follicular cycle in mice, preventing alopecia associated with its inactivation.

This review discusses hormonal influences on hair growth and suggests that understanding hormone-gene interactions may improve treatment of hirsutism and alopecia, but reports no new clinical findings.

In this study, eight patients with hereditary vitamin D-resistant rickets who share a specific VDR mutation showed improved clinical symptoms except alopecia after up to 11 years of treatment.

This study identified two distinct VDR gene mutations among Lebanese families with hereditary vitamin D-resistant rickets, noting varied treatment responses and promising outcomes despite severe phenotypes.

This study observed wide clinical diversity among five patients with the same VDR gene mutation causing vitamin D-dependent rickets type II, suggesting involvement of a nuclear accessory factor and a nongenomic action of the vitamin.

This study described the clinical and genetic features of two Iranian siblings with hereditary vitamin D resistant rickets, identifying a specific VDR gene mutation contributing to their symptoms.

This study found that VDR knockout mice exhibited muscle and motor impairments affecting locomotor behavior, while cognitive functions such as exploration, working memory, and anxiety appeared unaffected.

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

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 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.

Hairless protein helps control hair growth by regulating vitamin D receptor activity.

This study concluded that KLF4 is a crucial regulator of hair follicle stem cell quiescence and may work by interacting with multiple transcription factors to control related genes.

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.

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.

In this study involving genetically modified rats, researchers observed that specific mutations in the vitamin D receptor affect calcium levels and bone formation, emphasizing the receptor's role in maintaining healthy bone density and its importance in regulating hair cycle and skin health.