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This study concluded that the hairless protein interacts with the vitamin D receptor to repress transcription crucial for hair cycling, employing multiple protein interfaces and modulating chromatin structure.

This study identified complex regulatory elements and interactions involving the Hr gene and HR protein that are crucial for hair follicle formation and cycling in mammals.

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 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 demonstrated that mice lacking skin-specific RXRalpha expression developed hair follicle degeneration and alopecia, indicating the importance of RXRalpha/VDR heterodimers in maintaining hair follicle homeostasis.

This study found that the effects of the vitamin D receptor on hair follicle cycling in mice are independent of its ability to bind a hormone, with specific domain mutations influencing hair regrowth outcomes.

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.

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.

This study created a humanized mouse model of hereditary vitamin D-resistant rickets that lacks alopecia, indicating the mutant receptor's potential to explore the syndrome's characteristics beyond vitamin D binding.

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 identified interactions between Vitamin D and Msx1 regulation pathways, noting that Msx1 overexpression decreases Vitamin D receptor expression in odontoblastic cells.

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 showed that vitamin D receptor gene-deficient rats exhibit hair loss and skin abnormalities due to differences in gene and protein expression patterns, while ligand-independent VDR action is crucial for normal hair cycle maintenance and skin formation.

This review examines the role of Hairless, a nuclear receptor corepressor, in regulating Wnt signaling during hair cycling and reports no new clinical results.

This study identified a novel V26M mutation in the vitamin D receptor as the cause of hereditary vitamin D resistant rickets in a patient, characterized by severe rickets and an unusual pattern of alopecia.

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.

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

This study demonstrated that a ligand-independent action of the vitamin D receptor significantly affects keratinocyte behavior in hair follicles and skin, pointing to its crucial role in maintaining normal hair and skin structures in rats.

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

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.

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

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 review presents updated tables of mouse mutants with hair growth abnormalities to aid in understanding the molecular mechanisms of human hair disorders, but reports no new clinical results.

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 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 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.