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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 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 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 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.

In this study, synthetic vitamin D3 analogs stimulated hair growth and formation of normal hair follicles in nude mice, unlike the natural form 1,25 dihydroxyvitamin D3.

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

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.

Vitamin D3 affects cell differentiation in specific skin areas.

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 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 calcitriol, tacalcitol, and calcipotriol ointments achieved complete clearance of scalp psoriasis in 45%, 35.2%, and 17.6% of patients, respectively, with minimal side effects.

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.

This study identified three new mutations in the VDR ligand-binding domain that may cause dysfunction, and noted that oral calcium and calcidol treatment was effective, but only one patient experienced hair growth.

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.

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.

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 study observed that vitamin D receptor expression in certain hair follicle cells varies throughout the murine hair cycle, suggesting a potential role for 1,25-dihydroxyvitamin D3 in hair follicle biology.

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.

In this study, researchers identified a novel p.R50X mutation in the vitamin D receptor gene, linked to hereditary vitamin D-resistant rickets in two siblings.

This case study reports on a rare form of vitamin D resistant rickets in a 37-year-old male, highlighting the condition's clinical features and the necessity for a thorough understanding of calcium and vitamin D metabolism in the diagnosis and management of metabolic bone diseases.

This abstract reviews hereditary vitamin D-resistant rickets, a rare genetic condition causing severe early childhood rickets, and reports no new results; effective treatment typically requires high doses of calcium to address hypocalcemia and secondary hyperparathyroidism.

This paper discusses the use of Digital Volumetric Imaging with fluorescent dyes to visualize and compare the interior structures of six different virgin hair types, reporting no new clinical results.

In this study, researchers assessed vitamin D3 levels in adolescents, finding a suboptimal average of 22.00 ng/ml, and demonstrated that supplementing with 1000 IU/day of vitamin D3 significantly raised levels and improved physical and mental potential over two months.

This study found that 1,25-dihydroxyvitamin D3 promotes hair growth and regeneration in mice by prolonging the anagen phase and counteracting DHT's inhibitory effects, suggesting its potential therapeutic role for androgenetic alopecia.

This study found that a topical vitamin D3 analogue had an anti-proliferative effect on guinea pig skin epidermis.

This study suggests that vitamin D and its receptor may protect against the development of epidermal tumors following UV radiation by regulating specific cellular signaling pathways.

This report describes siblings with vitamin D-dependent rickets type 2, characterized by growth retardation, alopecia totalis, and low 25(OH)D3 levels, highlighting its autosomal recessive pattern and distinction from other rickets types.

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

This study characterized two siblings with hereditary vitamin D resistant rickets and a mutation in the vitamin D receptor, finding no immune-related disorders despite a defective T cell response to vitamin D.

This study found that certain VDR gene polymorphisms are more prevalent in female pattern hair loss patients than in healthy controls, suggesting these polymorphisms may increase disease risk.