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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 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 lower expression of VDR protein in breast cancer patients is associated with increased bone metastasis and poorer prognosis, making it a significant prognostic factor.

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 observed wide clinical diversity among five patients with the same VDR gene mutation causing vitamin D-dependent rickets type II, suggesting involvement of a nuclear accessory factor and a nongenomic action of the vitamin.

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.

This case report describes two siblings with gray patch tinea capitis, highlighting exposure to cats and inappropriate corticosteroid use as risk factors, and treatment with griseofulvin and terbinafine.

This study explored the expression and potential functions of long non-coding RNAs in the skin pigmentation of Koi carp, revealing their involvement in pigmentation and differentiation mechanisms.

This review discusses the multifaceted role of vitamin D in the body, noting its influence on calcium balance, hair cycle maintenance, cell proliferation, cardiovascular function, and immune modulation, with no new clinical results reported.

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.

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

This study suggests that while VDR is crucial for maintaining hair follicles in mice, their degeneration may be linked to impaired cell migration during hair growth phases rather than stem cell loss.

Lack of vitamin D receptor increases skin tumor risk by boosting hedgehog signaling.

This study found that mice lacking the vitamin D receptor (VDR) developed skin tumors more rapidly than those with normal VDR activity, regardless of 1,25-dihydroxyvitamin D(3) presence.

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.

This review discusses the role of the unliganded vitamin D receptor in hair follicle cycling and tumor formation in mice and reports no new experimental findings.

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 review discusses vitamin D and calcium signaling roles in epidermal stem cell processes essential for wound healing but reports no new experimental results, emphasizing their potential interdependent regulatory mechanisms.

In their mouse study, Oda et al. found that removing the MED1 gene in the skin led to hair loss and changes in epidermal cell differentiation, indicating MED1's significant role in these processes.

This study found that RXRα plays a critical role in hair cycling and keratinocyte functions in mice, likely through its interaction with VDR in epidermal cells.

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 article compares two rare genetic diseases, vitamin D-dependent rickets type 1 and type 2, focusing on their similar presentations of hypocalcemia and rickets in infancy, but reports no new clinical results.

This study found that absence of the vitamin D receptor in keratinocytes impairs canonical Wnt signaling and leads to alopecia due to defects in keratinocyte stem cells.

This case report describes a patient with mutations in both alleles of the vitamin D receptor who exhibited hair loss clinically indistinguishable from generalized atrichia with papules, suggesting a potential genetic pathway shared with the hairless gene.

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 article outlines the potential for upregulating the vitamin D receptor in treating hair disorders, emphasizing the need for further studies to evaluate vitamin D's role in the hair cycle.

This study suggests that vitamin D and calcium signaling play a crucial role in wound healing by regulating stem cell activation through enhanced β-catenin transcriptional activity in mice.

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 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.

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.