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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 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 showed disrupted hair follicle cycling, which was partially restored with hedgehog signaling pathway activation, suggesting a role for this pathway in follicle regulation independent of vitamin D.

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

This study found that c-Jun is essential for vitamin D receptor expression, and the vitamin D receptor inhibits c-Jun-dependent cell death through non-classical mechanisms independent of vitamin D3.

This study found that the novel drug VDC-1101 showed a 45% objective response rate in treating canine cutaneous T-cell lymphoma, offering a potential treatment option for this challenging disease.

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.

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 found that the absence of vitamin D receptor-mediated suppression of PPARγ expression causes hair loss in VDR-null mice.

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.

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 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 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.

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 Vdr-knockout mice experience hair cycle arrest during the catagen stage, leading to alopecia, with persistent epithelial strands forming in the hair follicles, indicating Vitamin D receptor's role in regulating hair follicle regression and regeneration.

In this study, researchers found no significant association between VDR gene polymorphisms and the susceptibility to alopecia areata, suggesting that these genetic variations may not play a role in the disease's development.

This study found that VDAC2 promotes apoptosis in secondary hair follicle stem cells of Albas cashmere goats by activating the P53 signaling pathway, with knockdown of VDAC2 reducing apoptosis and a P53 inhibitor partially rescuing VDAC2-induced apoptosis.

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 investigated genetic and epigenetic markers for prostate cancer, reporting that certain genotype combinations may influence cancer risk or protection and identifying GSTP1 promoter methylation as a strong prognostic and diagnostic marker linked to tumor aggressiveness.

This in-silico study identified several compounds as potential Vitamin D Receptor agonists, with Dolichosterone showing the strongest binding energy.

This study found that CYP11A1-derived vitamin D3 analogs inhibit fibroblast proliferation and decrease collagen production through VDR expression, showing potential antifibrotic and antiproliferative activity in human dermal fibroblasts.

This study observed that Vitamin D receptor expression at protein and mRNA levels was significantly lower in the hair follicles of alopecia areata patients compared to healthy individuals.

This article discusses the expression of vitamin D receptor in hair follicles and its role in alopecia, without presenting new findings; the authors highlight the involvement of Wnt/b-catenin signaling in hair growth.

This study found that p63 and p73 regulate the vitamin D receptor (VDR), with p63 influencing cancer cell behaviors and p73 playing a role in vitamin D-mediated differentiation.

This study found that the rs2228570 polymorphism of the VDR gene was associated with an increased risk of melanoma, while the rs731236 polymorphism was linked to a protective effect against the disease in Colombian patients.

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 report, a 23-year-old woman developed nephrotic syndrome and was diagnosed with lupus nephritis after receiving the first dose of the AstraZeneca COVID-19 vaccine, but causation is not established.