Search

everythingexperts & clinicslearnfaqsresearchcommunity

for

Search:↓

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.

Vitamin D3 affects cell differentiation in specific skin areas.

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 case study reports that a 3 ½ year-old male with vitamin D-dependent type II rickets showed partial improvement in alopecia and rickets when treated with high doses of 1,25(OH)2 vitamin D3.

This review highlights the crucial role of vitamin D signaling in epidermal stem cells during skin wound healing, emphasizing its distinct functions from calcium metabolism and its importance in genomic regulation mediated by the vitamin D receptor.

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.

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 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 case study describes a child with rickets and alopecia who responded to a small dose of 1-a-hydroxyvitamin D3, but her alopecia remained unchanged despite treatment.

In this study, researchers identified a unique Arg30stop mutation in the vitamin D receptor gene that causes hereditary vitamin D-resistant rickets in a young French-Canadian boy by truncating the receptor and causing hormone resistance.

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 found that VDR deficiency in mice leads to various skin pathologies but does not affect the phenotype or function of Langerhans cells.

This study suggests that 1,25-dihydroxyvitamin D(3) and fibroblast growth factor 23 form a crucial axis in regulating phosphate balance, akin to its role in calcium regulation, and explores novel VDR interactions including with curcumin.

Vitamin D3 may prevent hair loss from chemotherapy, but side effects and cancer cell protection are concerns.

In this mouse study, topical 1,25-dihydroxyvitamin D3 protected against cyclophosphamide-induced hair loss and inhibited mammary tumor growth, with effects varying by sex and tumor presence.

This study found that obese Egyptian women with polycystic ovary syndrome had significantly lower serum 25-OH vitamin D levels compared to non-obese women with the condition.

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 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 found that mice lacking the 1αOHase enzyme, which is responsible for producing a key vitamin D metabolite, showed impaired epidermal differentiation and delayed recovery of skin barrier function after disruption.

This minireview discusses a proposed model of the vitamin D receptor that explains how 1alpha,25(OH)2D3 can mediate both genomic and rapid responses through different ligand shapes and cellular locations, without presenting new research findings.

This review summarizes the proposed model that describes how different shapes of 1alpha,25(OH)2D3 ligands interact with the vitamin D receptor to mediate genomic and rapid responses in cells.

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.

This review examines the functions of vitamin D and its receptor in skin and explores how these are regulated, reporting no new clinical results.

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 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 measuring 24-OHase induction by 1,25(OH)2D3 in cultured skin fibroblasts is a sensitive test for detecting genetic defects in the 1,25(OH)2D effector pathway.

This case report discusses a 27-month-old girl with vitamin D-dependent rickets type II, who showed minor improvement in skeletal features and alopecia after high-dose oral calcium and vitamin D3 treatment.

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 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 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.