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.
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research Deletion of DNA Binding Domain of the Vitamin D Receptor Abrogates Genomic and Nongenomic Functions of Vitamin D
Removing part of the vitamin D receptor stops vitamin D from working properly.
research Does Vitamin D Play a Role in Msx1 Homeoprotein Expression Involving an Endogenous Antisense mRNA?
Vitamin D affects Msx1 protein expression and may influence mineralized tissue health.
research In Vivo Function of VDR in Gene Expression: VDR Knock-Out Mice
Vitamin D receptor is crucial for bone health and mineral metabolism.
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 Regulation of VDR by ΔNp63α Is Associated with Inhibition of Cell Invasion
ΔNp63α helps control a protein that stops cancer cells from spreading.
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 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 Hairless and Wnt Signaling: Allies in Epithelial Stem Cell Differentiation
The HR protein's role as a repressor is essential for controlling hair growth.
research Disruption of the Hedgehog Signaling Pathway Contributes to Hair Follicle Cycling Deficiency in VDR Knockout Mice
Mice without Vitamin D receptors have hair growth problems because of issues in the hedgehog signaling pathway.
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 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 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 Hairless Is a Nuclear Receptor Corepressor Essential for Skin Function
Hairless protein is crucial for healthy skin and hair, and its malfunction can cause hair loss.
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 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.
research Mutant Laboratory Mice With Abnormalities in Hair Follicle Morphogenesis, Cycling, and Structure: An Update
The document concludes that mouse models are crucial for studying hair biology and that all mutant mice may have hair growth abnormalities that require detailed analysis to identify.
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 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 Mutations in the Vitamin D Receptor and Hereditary Vitamin D-Resistant Rickets
Mutations in the vitamin D receptor cause hereditary vitamin D-resistant rickets, leading to poor bone health and requiring high calcium doses for treatment.
research Roles of MED1 in Quiescence of Hair Follicle Stem Cells and Maintenance of Normal Hair Cycling
MED1 is essential for normal hair growth and maintaining hair follicle stem cells.
research Physiological and Retinoid-Induced Proliferations of Epidermis Basal Keratinocytes Are Differently Controlled
Normal skin cell renewal doesn't need RAR signaling, but vitamin A-related skin thickening does.
research Hairless: A Nuclear Receptor Corepressor Essential for Skin Function
The Hairless gene is crucial for healthy skin and hair growth.
research Mesenchymal–Epithelial Interactions During Hair Follicle Morphogenesis and Cycling
The conclusion is that certain cell interactions and signals are crucial for hair growth and regeneration.
research Study of Gene Expression Alteration in Male Androgenetic Alopecia: Evidence of Predominant Molecular Signaling Pathways
Hair loss involves immune responses, inflammation, and disrupted signaling pathways.
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 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 Gene Therapy for Alopecia in Type II Rickets Model Rats Using Vitamin D Receptor-Expressing Adenovirus Vector
Gene therapy helped rats with a specific type of rickets grow hair without severe inflammation.
research The Hair Follicle as a Dynamic Mini-Organ
Hair follicles are complex, dynamic mini-organs that help us understand cell growth, death, migration, and differentiation, as well as tissue regeneration and tumor biology.
research The Hair Follicle as an Estrogen Target and Source
Estrogens significantly influence hair growth by interacting with receptors in hair follicles and may help regulate the hair growth cycle.