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- The peach RGF/GLV signalling peptide pCTG134 is involved in a regulatory circuit that sustains auxin and ethylene actions
- The Peach RGF/GLV Signaling Peptide pCTG134 Is Involved in a Regulatory Circuit That Sustains Auxin and Ethylene Actions
- ETHYLENE AND PHOSPHORUS RESPONSES IN PLANTS
- Synthesis and 5α-Reductase Inhibitory Activity of C21 Steroids Having 1,4-diene or 4,6-diene 20-ones and 4-Azasteroid 20-Oximes
- 25 Hydroxyvitamin D 1 α-Hydroxylase Is Required for Optimal Epidermal Differentiation and Permeability Barrier Homeostasis
- 1,25-dihydroxyvitamin D resistance, rickets, and alopecia
- ANALYSIS OF THE RELATION BETWEEN ALOPECIA AND RESISTANCE TO 1,25‐DIHYDROXYVITAMIN D
- Noncalcemic actions of 1,25-dihydroxyvitamin D3 and clinical applications
- Hair follicle expression of 1,25-dihydroxyvitamin D3 receptors during the murine hair cycle
- Rickets and Alopecia with Resistance to 1,25-Dihydroxyvitamin D: Two Different Clinical Courses with Two Different Cellular Defects*
- VITAMIN D RESISTANT RICKETS WITH ALOPECIA: A FORM OF END ORGAN RESISTANCE TO 1,25 DIHYDROXY VITAMIN D
- Vitamin D-dependent rickets type II. Defective induction of 25-hydroxyvitamin D3-24-hydroxylase by 1,25-dihydroxyvitamin D3 in cultured skin fibroblasts.
- Topographical and developmental studies on target sites of 1,25 (OH2) vitamin D3 in skin
- Hereditary 1,25-Dihydroxyvitamin D Resistant Rickets due to a Mutation Causing Multiple Defects in Vitamin D Receptor Function
- GLP-1 Receptor Agonists: Beyond Their Pancreatic Effects
- The effects of minoxidil, 1% pyrithione zinc and a combination of both on hair density: a randomized controlled trial
- 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
- Vitamin D-dependent rickets type II: extreme end organ resistance to 1,25-dihydroxy vitamin D3 in a patient without alopecia
- 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
- Analysis of 1,25-Dihydroxyvitamin D3 Receptors (VDR. in Basal Cell Carcinomas
- Proliferation and Differentiation of Cultured Human Keratinocytes is Modulated by 1,25(OH)<sub>2</sub>D<sub>3</sub> and Synthetic Vitamin D<sub>3</sub> Analogues in a Cell Density‐, Calcium‐ and Serum‐Dependent Manner*
- The vitamin D receptor functions as a transcription regulator in the absence of 1,25-dihydroxyvitamin D3
- A unique insertion/duplication in the VDR gene that truncates the VDR causing hereditary 1,25-dihydroxyvitamin D-resistant rickets without alopecia
- 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
- Evidence for 1,25-Dihydroxyvitamin D3-independent Transactivation by the Vitamin D Receptor
- Hereditary 1,25‐Dihydroxyvitamin D‐Resistant Rickets in a Pomeranian Dog Caused by a Novel Mutation in the Vitamin D Receptor Gene
- Hereditary 1,25-Dihydroxyvitamin D-Resistant Rickets
- 1 Androgens
- Biphasic Effect of 1,25-Dihydroxyvitamin D3 on Human Hair Follicle Growth and Hair Fiber Production in Whole-Organ Cultures