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Research 91–120 of 486
- Does D matter? The role of vitamin D in hair disorders and hair follicle cycling
- Hair follicle expression of 1,25-dihydroxyvitamin D3 receptors during the murine hair cycle
- Vitamin D and calcium regulation of epidermal wound healing
- Development and progression of alopecia in the vitamin D receptor null mouse
- Hairless Suppresses Vitamin D Receptor Transactivation in Human Keratinocytes
- Hairless and Wnt Signaling: Allies in Epithelial Stem Cell Differentiation
- The role of nuclear hormone receptors in cutaneous wound repair
- Hereditary 1,25-Dihydroxyvitamin D Resistant Rickets due to a Mutation Causing Multiple Defects in Vitamin D Receptor Function
- Quantification of the Vitamin D Receptor−Coregulator Interaction
- Vitamin D and androgen receptor-targeted therapy for triple-negative breast cancer
- Targeted Expression of Human Vitamin D Receptor in the Skin Promotes the Initiation of the Postnatal Hair Follicle Cycle and Rescues the Alopecia in Vitamin D Receptor Null Mice
- Vitamin D‐dependent rickets type I and type II
- The Vitamin D Receptor Is Required for Activation of cWnt and Hedgehog Signaling in Keratinocytes
- Ligand-Dependent Actions of the Vitamin D Receptor Are Required for Activation of TGF-β Signaling during the Inflammatory Response to Cutaneous Injury
- The Vitamin D Receptor as Tumor Suppressor in Skin
- Role of the vitamin D receptor in hair follicle biology
- Vitamin D Receptor, UVR, and Skin Cancer: A Potential Protective Mechanism
- Molecular Genetic and Endocrine Mechanisms of Hair Growth
- The hair cycle and Vitamin D receptor
- Hereditary 1,25-dihydroxyvitamin D-resistant rickets with alopecia resulting from a novel missense mutation in the DNA-binding domain of the vitamin D receptor
- Reciprocal role of vitamin D receptor on β-catenin regulated keratinocyte proliferation and differentiation
- Tryptophan Missense Mutation in the Ligand‐Binding Domain of the Vitamin D Receptor Causes Severe Resistance to 1,25‐Dihydroxyvitamin D
- Hereditary 1,25‐Dihydroxyvitamin D–Resistant Rickets Due to an Opal Mutation Causing Premature Termination of the Vitamin D Receptor
- Vitamin D Receptor Is Required for Proliferation, Migration, and Differentiation of Epidermal Stem Cells and Progeny during Cutaneous Wound Repair
- Vitamin D resistance
- The vitamin D receptor functions as a transcription regulator in the absence of 1,25-dihydroxyvitamin D3
- Hereditary vitamin D-resistant rickets (HVDRR) owing to a heterozygous mutation in the vitamin D receptor
- Two New Unrelated Cases of Hereditary 1,25-Dihydroxyvitamin D-resistant Rickets with Alopecia resulting from the same Novel Nonsense Mutation in the Vitamin D Receptor Gene
- Vitamin D receptor polymorphisms and the polycystic ovary syndrome: A systematic review
- Hairless is a nuclear receptor corepressor essential for skin function