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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 Hairless (Hr) acts as a corepressor of the vitamin D receptor (VDR) in human keratinocytes, blocking the action of vitamin D on keratinocyte differentiation.

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.

This study found that the protein hairless acts as both a corepressor and coactivator of the vitamin D receptor, influencing gene transcription in a ligand-selective manner.

This study identified a novel I268T mutation in the vitamin D receptor that reduces its function, contributing to hereditary vitamin D-resistant rickets, and found that a potent vitamin D analog could improve receptor function.

This study found that the hairless gene product (Hr) suppresses VDR-mediated gene activation by directly interacting with the vitamin D receptor, potentially affecting hair follicle function.

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 hair follicle homeostasis in mice requires vitamin D receptor expression in keratinocytes, independent of its ligand activation.

This study found that the mutant hairless rhino bald protein in mice interacts with the vitamin D receptor but cannot repress its transactivation and shows abnormal cellular localization.

This study demonstrated that both HR isoforms are expressed in keratinocytes, but HRDelta1072-1126 lacks corepressor activity and may act as a coactivator by inhibiting HDAC recruitment to the VDR transcriptional complex.

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

This study found that a hypomorphic mutation in the Hr gene contributes to the development of diet-induced pruritic atopic skin in mice, particularly when combined with dietary deficiencies of polyunsaturated fatty acids and starch.

The mutation causes hairless mice due to mislocalized and dysfunctional HR protein.

This study found that a specific VDR amino acid substitution in children with hereditary vitamin D-resistant rickets disrupts ligand binding and gene activation but does not impair hair follicle development.

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 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 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 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 identified the Hairless (Hr) gene-encoded protein as a corepressor that plays a crucial role in maintaining skin and hair by regulating epithelial stem cell differentiation and gene expression via chromatin remodeling, which may impact both development and 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.

This study found that a novel missense mutation in the vitamin D receptor caused hereditary 1,25-dihydroxyvitamin D-resistant rickets with alopecia by disrupting protein function, highlighting the importance of DNA binding in hair development.

This study found that most pathogenic HR mutants associated with atrichia with papular lesions had abolished corepressor activity due to defective interactions with histone deacetylases.

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

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 review discusses recent advances in molecular genetics and their impact on the accuracy and understanding of diagnosing inherited skin diseases but reports no new results.

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.