The Vitamin D Receptor Functions as a Transcription Regulator in the Absence of 1,25-Dihydroxyvitamin D3

    Lee Seong Min, Pike J. Wesley
    Studysummary This study found that in a mouse model with hereditary 1,25-dihydroxyvitamin D resistant rickets, a mutant vitamin D receptor lacking hormone-binding ability could restore normal hair cycling and affect parathyroid hormone regulation.
    Automatically generated from the study's abstract, not written by a person, and not a review of the full paper. Not medical advice or a treatment recommendation. Read the original study, and consult a qualified healthcare professional before changing treatment. Full disclaimer
    Read the full study on sciencedirect.com →
    Discuss this study in the Community →

    Research cited in this study 5

    1. A Humanized Mouse Model of Hereditary 1,25-Dihydroxyvitamin D–Resistant Rickets Without Alopecia Endocrinology · 2014
    2. Mutations in the Vitamin D Receptor and Hereditary Vitamin D-Resistant Rickets BoneKEy Reports · 2014
    3. Vitamin D and the Skin: Physiology and Pathophysiology Reviews in endocrine and metabolic disorders · 2011
    4. Ligand-Independent Actions of the Vitamin D Receptor Maintain Hair Follicle Homeostasis Molecular Endocrinology · 2004
    5. Deletion of DNA Binding Domain of the Vitamin D Receptor Abrogates Genomic and Nongenomic Functions of Vitamin D Molecular Endocrinology · 2002