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Research 31–60 of 474
- Metabolic and cellular analysis of alopecia in vitamin D receptor knockout mice
- The Vitamin D Receptor Is a Wnt Effector that Controls Hair Follicle Differentiation and Specifies Tumor Type in Adult Epidermis
- Normalization of Mineral Ion Homeostasis by Dietary Means Prevents Hyperparathyroidism, Rickets, and Osteomalacia, But Not Alopecia in Vitamin D Receptor-Ablated Mice
- Targeting Expression of the Human Vitamin D Receptor to the Keratinocytes of Vitamin D Receptor Null Mice Prevents Alopecia
- Evaluation of Keratinocyte Proliferation and Differentiation in Vitamin D Receptor Knockout Mice*
- Mechanism of Vitamin D Receptor Action
- The role of vitamin D receptor mutations in the development of alopecia
- Mutations in the vitamin D receptor and hereditary vitamin D-resistant rickets
- Cloning of a Functional Vitamin D Receptor from the Lamprey (Petromyzon marinus), an Ancient Vertebrate Lacking a Calcified Skeleton and Teeth
- Overexpression of Hedgehog Signaling Is Associated with Epidermal Tumor Formation in Vitamin D Receptor–Null Mice
- Hair follicle expression of 1,25-dihydroxyvitamin D3 receptors during the murine hair cycle
- Development and progression of alopecia in the vitamin D receptor null mouse
- Hairless Suppresses Vitamin D Receptor Transactivation in Human Keratinocytes
- In vivo function of VDR in gene expression-VDR knock-out mice
- 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
- 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
- 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
- Disruption of the hedgehog signaling pathway contributes to the hair follicle cycling deficiency in Vdr knockout mice
- Vitamin D Receptor, UVR, and Skin Cancer: A Potential Protective Mechanism
- 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
- 1α,25(OH)2-Dihydroxyvitamin D3/VDR protects the skin from UVB-induced tumor formation by interacting with the β-catenin pathway