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This study observed that Cyp27b1−/− mice exhibited growth and skeletal abnormalities similar to those of Vdr−/− mice, despite differences like the development of alopecia in Vdr−/− mice, suggesting that 1α,25D3 may directly influence chondrocyte proliferation and differentiation.

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 study suggests that the vitamin D receptor and hairless gene may directly regulate each other via a transcriptional mechanism, potentially explaining phenotypic similarities between atrichia and VDRRIIa rickets.

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.

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 vitamin D regulates cholesterol metabolism and may influence prostate cancer development through mechanisms affecting prostate cell growth and sex hormone metabolism.

In this study, researchers observed that dietary vitamin D intake and light exposure play a crucial role in vitamin D metabolism in mice, suggesting similar importance for human health in maintaining optimal vitamin D levels.

The testes significantly contribute to vitamin D metabolism and may affect male reproductive health and conditions like hair loss.

This review highlights that vitamin D is increasingly recognized for its roles in skin health, including treatment of psoriasis, potential applications in conditions like atopic dermatitis, and possible prevention of skin malignancies, as observed in various studies linking low levels to autoimmune skin diseases.

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

This study suggests that unliganded vitamin D receptors in mice may cause more severe skeletal and mineral ion defects than VDR-null conditions, and vitamin D analogues may restore function in specific VDR mutations.

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.

In this study, researchers observed that the absence of the vitamin D receptor or its ligand-activated transcription in mice did not affect glucose homeostasis or gene expression in islets.

This article discusses the development and clinical progress of PROTAC technology, particularly focusing on the New Drug Application for vepdegestrant, an estrogen receptor-targeting PROTAC, marking significant advancements in targeted protein degradation therapies.

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 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 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 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 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, gene therapy using a VDR-expressing adenoviral vector promoted hair growth in Vdr-KO rats, suggesting its potential for treating alopecia associated with type II rickets.

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 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 found that VDR deficiency in mice leads to various skin pathologies but does not affect the phenotype or function of Langerhans cells.

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.

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 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.

In this study, researchers found that certain vitamin D receptor gene polymorphisms are significantly related to insulin concentration during a glucose tolerance test in young women with hyperandrogenism, but these polymorphisms did not affect bone metabolism or other biochemical parameters.

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.

This pilot clinical study introduces DEC cells as a novel therapy for Duchenne muscular dystrophy, confirming safety and efficacy in seven patients up to 24 months post-treatment.