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Research 91–120 of 1000+
- 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
- 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
- Hydroxyl radical mediates cisplatin-induced apoptosis in human hair follicle dermal papilla cells and keratinocytes through Bcl-2-dependent mechanism
- Autosomal Recessive Hypotrichosis with Woolly Hair Caused by a Mutation in the Keratin 25 Gene Expressed in Hair Follicles
- 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
- Overexpression of Bcl-2 Protects from Ultraviolet B-Induced Apoptosis but Promotes Hair Follicle Regression and Chemotherapy-Induced Alopecia
- Hereditary 1,25‐Dihydroxyvitamin D–Resistant Rickets Due to an Opal Mutation Causing Premature Termination of the Vitamin D Receptor
- 1α,25(OH)2-Dihydroxyvitamin D3/VDR protects the skin from UVB-induced tumor formation by interacting with the β-catenin pathway
- Analysis of 1,25-Dihydroxyvitamin D3 Receptors (VDR. in Basal Cell Carcinomas
- Expression of Cyclooxygenase Isozymes During Morphogenesis and Cycling of Pelage Hair Follicles in Mouse Skin: Precocious Onset of the First Catagen Phase and Alopecia upon Cyclooxygenase-2 Overexpression
- Normal Fur Development and Sebum Production Depends on Fatty Acid 2-Hydroxylase Expression in Sebaceous Glands
- 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
- Interleukin-25-Mediated-IL-17RB Upregulation Promotes Cutaneous Wound Healing in Diabetic Mice by Improving Endothelial Cell Functions
- The hair growth promoting effect of ascorbic acid 2-phosphate, a long-acting Vitamin C derivative
- 1α,25-Dihydroxyvitamin D3 Modulates the Hair-Inductive Capacity of Dermal Papilla Cells: Therapeutic Potential for Hair Regeneration
- Hereditary 1,25‐Dihydroxyvitamin D‐Resistant Rickets in a Pomeranian Dog Caused by a Novel Mutation in the Vitamin D Receptor Gene
- Serum lipocalin-2 as an insulin resistance marker in patients with polycystic ovary syndrome
- Hereditary 1,25-Dihydroxyvitamin D-Resistant Rickets
- PCOS in Adolescence and Type 2 Diabetes
- Gene expression of type 2 17β hydroxysteroid dehydrogenase in scalp hairs of hirsute women
- Biphasic Effect of 1,25-Dihydroxyvitamin D3 on Human Hair Follicle Growth and Hair Fiber Production in Whole-Organ Cultures
- A Humanized Mouse Model of Hereditary 1,25-Dihydroxyvitamin D–Resistant Rickets Without Alopecia