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Research 181–210 of 479
- VITAMIN D DEPENDENT RICKETS TYPE II (VDR-11). RESPONSE TO PROLONGED THERAPY WITH NOCTURNAL CALCIUM INFUSIONS
- Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice
- Vitamin D Receptor: New Assignments for an Already Busy Receptor
- Vitamin D receptor: molecular signaling and actions of nutritional ligands in disease prevention
- Vitamin D and the skin: Physiology and pathophysiology
- Ligand-Independent Actions of the Vitamin D Receptor Maintain Hair Follicle Homeostasis
- Vitamin D Receptor: Key Roles in Bone Mineral Pathophysiology, Molecular Mechanism of Action, and Novel Nutritional Ligands
- 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
- Cloning of a Functional Vitamin D Receptor from the Lamprey (Petromyzon marinus), an Ancient Vertebrate Lacking a Calcified Skeleton and Teeth
- 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 and Wnt Signaling: Allies in Epithelial Stem Cell Differentiation
- 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
- 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
- Interactions of the Vitamin D Receptor with the Corepressor Hairless
- 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
- Lymphoid Enhancer-binding Factor-1 (LEF1) Interacts with the DNA-binding Domain of 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