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Research 31–60 of 1000+
- Hereditary 1,25-Dihydroxyvitamin D Resistant Rickets due to a Mutation Causing Multiple Defects in Vitamin D Receptor Function
- 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
- Hereditary 1,25‐Dihydroxyvitamin D–Resistant Rickets Due to an Opal Mutation Causing Premature Termination of the Vitamin D Receptor
- 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
- Hereditary 1,25‐Dihydroxyvitamin D‐Resistant Rickets in a Pomeranian Dog Caused by a Novel Mutation in the Vitamin D Receptor Gene
- Tooth Development Associated with Mutations in Hereditary Vitamin D–Resistant Rickets
- A human vitamin D receptor mutation causes rickets and impaired Th1/Th17 responses
- Novel Vitamin D Receptor Mutations in Hereditary Vitamin D Resistant Rickets in Chinese
- Hereditary 1,25-dihydroxyvitamin D-resistant rickets with alopecia in four Egyptian families: report of three novel mutations in the vitamin D receptor gene
- Hereditary Vitamin D Resistant Rickets: Clinical, Laboratory, and Genetic Characteristics of 2 Iranian Siblings
- Type II Vitamin D Dependent Rickets: A Case Report
- Gene therapy for alopecia in type II rickets model rats using vitamin D receptor-expressing adenovirus vector
- Two siblings with vitamin-D-dependent rickets type II: No recurrence of rickets for 14 years after cessation of therapy
- Experience of intravenous calcium treatment and long-term responses to treatment in a patient with hereditary vitamin D-resistant rickets resulting from a novel mutation
- Mutations in the vitamin D receptor gene in four patients with hereditary 1,25-dihydroxyvitamin D-resistant rickets
- Editorial: Vitamin D 1α-Hydroxylase Knockout Mice as a Hereditary Rickets Animal Model
- Persistent hyperparathyroidism in vitamin D-dependent rickets type 2A does not prevent normalization of hypophosphatemia or healing of the rickets
- Normalization of Mineral Ion Homeostasis by Dietary Means Prevents Hyperparathyroidism, Rickets, and Osteomalacia, But Not Alopecia in Vitamin D Receptor-Ablated Mice<sup>1</sup>
- Normalization of Mineral Ion Homeostasis by Dietary Means Prevents Hyperparathyroidism, Rickets, and Osteomalacia, But Not Alopecia in Vitamin D Receptor-Ablated Mice
- The combined use of intravenous and oral calcium for the treatment of vitamin D dependent rickets type II (VDDRII)
- The effect of 1,25-dihydroxyvitamin D3 on the growth and differentiation of cultured human outer root sheath cells from normal subjects and patients with vitamin D-dependent rickets type II with alopecia
- Genetic Disorders and Defects in Vitamin D Action
- Atrichia Caused by Mutations in the Vitamin D Receptor Gene is a Phenocopy of Generalized Atrichia Caused by Mutations in the Hairless Gene
- A unique insertion/duplication in the VDR gene that truncates the VDR causing hereditary 1,25-dihydroxyvitamin D-resistant rickets without alopecia
- Vitamin D and the Parenteral Nutrition Patient
- 4 Vitamin D resistance
- Ligand‐independent Regulation of the hairless Promoter by Vitamin D Receptor<sup>†</sup>
- Clinical and Genetic Characterization of Tunisian Children with Hereditary 1,25-Dihydroxyvitamin D-Resistant Rickets
- Rickets with alopecia-remission following a course of 1-?-hydroxy vitamin D3 therapy