research Hairless Suppresses Vitamin D Receptor Transactivation in Human Keratinocytes
Hairless protein can block vitamin D activation in skin cells.
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30 / 393 resultsresearch The Impact of VDR Expression and Regulation In Vivo
VDR regulation varies by tissue and is crucial for its biological functions.
research Ligand-Independent Actions of Vitamin D Receptor
The vitamin D receptor helps maintain hair and bone health even without binding vitamin D.
research The Vitamin D Receptor Is a Wnt Effector That Controls Hair Follicle Differentiation and Specifies Tumor Type in Adult Epidermis
Vitamin D receptor helps control hair growth and could be used to treat certain skin tumors.
research Evidence for 1,25-Dihydroxyvitamin D3-Independent Transactivation by the Vitamin D Receptor
The vitamin D receptor can work without its usual activating molecule.
research Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice
Mice without the vitamin D receptor have bone issues and other health problems, suggesting vitamin D is important for preventing various diseases in humans.
research Vitamin D Receptor: Molecular Signaling and Actions of Nutritional Ligands in Disease Prevention
Vitamin D receptor interacts with certain dietary components to help prevent diseases and regulate hair growth.
research Hairless Modulates Ligand-Dependent Activation of the Vitamin D Receptor-Retinoid X Receptor Heterodimer
Hairless protein can both repress and activate vitamin D receptor functions, affecting gene regulation.
research Functional Analysis of VDR Gene Mutation R343H in a Child with Vitamin D-Resistant Rickets with Alopecia
The R343H mutation in the VDR gene causes vitamin D-resistant rickets with alopecia by impairing specific gene activity.
research Vitamin D: More Than a Bona Fide Hormone
Vitamin D is important for bones, hair, blood pressure, and breast development.
research Vitamin D Receptor-Mediated Control of Soggy, Wise, and Hairless Gene Expression in Keratinocytes
Vitamin D receptor helps control hair growth genes in skin cells.
research Stress-Induced c-Jun-Dependent Vitamin D Receptor Activation Dissects the Non-Classical VDR Pathway from the Classical VDR Activity
Stress activates a special function of the Vitamin D receptor with the help of c-Jun, which can also prevent cell death.
research Vitamin D Metabolism and Function in the Skin
Skin cells produce and activate vitamin D, which regulates skin functions and supports hair growth.
research DNA Damage-Inducible Transcript 4 Is an Innate Surveillant of Hair Follicular Stress in Vitamin D Receptor Knockout Mice and a Regulator of Wound Re-Epithelialization
Vitamin D receptor is important for regulating hair growth and wound healing in mice.
research Coactivator MED1 Ablation in Keratinocytes Results in Hair-Cycling Defects and Epidermal Alterations
Deleting MED1 in skin cells causes hair loss and skin changes.
research Interactions of the Vitamin D Receptor with the Corepressor Hairless
Most Hairless gene mutations reduce its ability to work with the Vitamin D Receptor, which might explain a certain type of hair loss.
research Vitamin D and the Skin: Physiology and Pathophysiology
Vitamin D and its receptor regulate skin functions like cell growth, immunity, hair cycle, and tumor prevention.
research Lymphoid Enhancer-Binding Factor-1 Interacts with the DNA-Binding Domain of the Vitamin D Receptor
LEF1 interacts with Vitamin D Receptor, affecting hair follicle regeneration and this could be linked to hair loss conditions.
research Polymorphisms in Androgen and Estrogen Receptor Genes: Effects on Male Aging
Changes in testosterone and estrogen receptor genes can affect how men age, influencing body fat, hair patterns, and possibly leading to skin disorders.
research The Nuclear Vitamin D Receptor: Biological and Molecular Regulatory Properties Revealed
The vitamin D receptor is crucial for bone health and affects various body systems, with mutations potentially leading to disease.
research Hereditary 1,25-Dihydroxyvitamin D-Resistant Rickets (HVDRR): Clinical Heterogeneity and Long-Term Efficacious Management of Eight Patients from Four Unrelated Arab Families with a Loss of Function VDR Mutation
Patients with the same genetic mutation for vitamin D-resistant rickets showed different symptoms but all improved with treatment except for hair loss.
research Genetic Dissection of Retinoic Acid Function in Epidermis Physiology
Retinoic acid affects skin and hair health by working with specific receptors, and its absence can lead to hair loss and skin changes.
research Ligand-Independent Actions of the Vitamin D Receptor: More Questions Than Answers
The vitamin D receptor can act without its usual activating molecule, affecting hair growth and skin cancer, but its full range of actions is not well understood.
research Genetic Disorders and Defects in Vitamin D Action
Two rare genetic diseases cause severe rickets in children due to defects in vitamin D metabolism.
research Quantification of the Vitamin D Receptor-Coregulator Interaction
Vitamin D receptor binds similarly to natural and synthetic ligands, affecting gene regulation.
research Combined Deletion of the Vitamin D Receptor and Calcium-Sensing Receptor Delays Wound Re-Epithelialization
Removing vitamin D and calcium receptors in mice skin cells slows down skin wound healing.
research Clinical and Genetic Findings in a Chinese Family with VDR-Associated Hereditary Vitamin D-Resistant Rickets
A Chinese family had a child with a specific gene mutation causing vitamin D-resistant rickets, but the child improved with calcium and low-dose calcitriol.
research Vitamin D Resistance
Vitamin D and its receptor are essential for hair growth, cell regulation, immune function, and heart health.
research Dermatopathology and Molecular Genetics
Combining skin tissue pathology with genetics has greatly improved the diagnosis and understanding of certain skin diseases.
research Ligand-Independent Regulation of the Hairless Promoter by Vitamin D Receptor
Vitamin D receptor can control the hairless gene linked to hair loss even without vitamin D.