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This study found that a novel R343H mutation in the vitamin D receptor gene impairs its transcription activity, contributing to hereditary vitamin D-resistant rickets and alopecia in the affected family.

This study found that both the natural ligand 1alpha,25(OH)(2)D(3) and the synthetic agonist LG190178 bind similarly to the vitamin D receptor's coregulator motifs, suggesting similar biological functions.

In this case study, a girl with hereditary vitamin D resistant rickets had a novel mutation in the VDR gene that affected hair cycling without causing total alopecia, suggesting ligand-independent VDR function in hair cycling.

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 suggests that 1,25-dihydroxyvitamin D(3) and fibroblast growth factor 23 form a crucial axis in regulating phosphate balance, akin to its role in calcium regulation, and explores novel VDR interactions including with curcumin.

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 found that ΔNp63α directly regulates VDR expression, which in turn may reduce invasiveness in an epidermoid cancer cell line.

This review discusses inherited forms of vitamin D-dependent rickets and explains their genetic and metabolic causes but reports no new clinical findings.

This review summarizes the proposed model that describes how different shapes of 1alpha,25(OH)2D3 ligands interact with the vitamin D receptor to mediate genomic and rapid responses in cells.

This study found that the vitamin D receptor in lampreys, which lack bones and hair, binds 1,25-dihydroxyvitamin D3 and may function to induce enzymes for detoxifying substances.

This case report details a severe instance of VDR-II where intravenous calcium infusions, administered nightly, successfully improved clinical, radiological, and biochemical signs of rickets without alopecia despite ineffective calcitriol therapy.

In this study, a novel VDR gene mutation was identified in a child with HVDRR, and the researchers observed that high-dose intravenous calcium therapy led to significant and sustained improvement in rickets symptoms.

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 found that DVd therapy is at least as effective as VAD/VAd for treating multiple myeloma and causes fewer side effects and reduced hospital visits.

This study found that the vitamin D-VDR system is crucial for mineral and bone metabolism post-weaning and identified missense mutations in 1alpha-hydroxylase causing type I rickets.

This study found that deleting β-catenin in epidermis-specific VDR knockout mice did not prevent UVB-induced skin tumors, indicating β-catenin does not compensate for VDR's role in tumor suppression.

This minireview discusses a proposed model of the vitamin D receptor that explains how 1alpha,25(OH)2D3 can mediate both genomic and rapid responses through different ligand shapes and cellular locations, without presenting new research findings.

This study highlights the complex role of the vitamin D receptor in skin processes, where its disruption, along with calcium and co-regulator imbalances, could contribute to skin cancer development by altering skin differentiation and hair follicle cycling.

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.

This review explores how vitamin D3 analogs could target various skin processes and diseases, potentially offering selective and effective treatments beyond psoriasis, but reports no new clinical findings.

This abstract discusses two types of hereditary vitamin D metabolism defects, VDDR I and VDDR II, and reports on their distinct characteristics and treatment responses, without presenting new clinical data.

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.

In this study, a Chinese Han family with hereditary vitamin D-resistant rickets was found to have a homozygous missense mutation in the VDR gene, and the affected individual uniquely responded well to treatment with oral calcium and low-dose calcitriol.

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.

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 study found that basal cell carcinomas show strong expression of vitamin D receptors at both mRNA and protein levels, suggesting a potential role in tumor growth regulation.

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.

This article outlines the potential for upregulating the vitamin D receptor in treating hair disorders, emphasizing the need for further studies to evaluate vitamin D's role in the hair cycle.

This study indicates that vitamin D3 administration may protect rat hair follicles from radiation-induced damage, as evidenced by maintained follicle numbers and increased Vitamin D receptor activity in treated skin.

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.