research [Genetic expression and morphogenesis of the skin in vertebrates].
Retinoic acid can change skin structures in vertebrates, like turning scales into feathers or hair buds into glands.
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330-360 / 1000+ resultsresearch [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 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 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 A new mutation Rim3 resembling Re den is mapped close to retinoic acid receptor alpha (Rara) gene on mouse Chromosome 11
research Increased expression of Ectodysplasin A2 Receptor EDA2R is the most remarkable and ubiquitous aging-related transcriptional hallmark
The most common sign of aging at the gene level is more Ectodysplasin A2 Receptor (EDA2R) being made.
research Isolation and Characterization of Human Repetin, a Member of the Fused Gene Family of the Epidermal Differentiation Complex
Repetin is a protein involved in skin and hair development, binding calcium and compensating for other proteins when needed.
research Quantification of the Vitamin D Receptor−Coregulator Interaction
Vitamin D receptor binds similarly to natural and synthetic ligands, affecting gene regulation.
research Subcellular localization of the five members of the human steroid 5α-reductase family
All five human steroid 5α-reductase enzymes are found in the endoplasmic reticulum.
research Conditional expression of the ErbB2 oncogene elicits reversible hyperplasia in stratified epithelia and up-regulation of TGFα expression in transgenic mice
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 ERG induces androgen receptor-mediated regulation of SOX9 in prostate cancer
ERG increases SOX9, promoting prostate cancer growth and invasion.
research Androgen receptor-mediated gene activation in prostate cancer cells
Androgen receptors help prostate cancer cells grow and resist drugs.
research Physical and Functional Interaction between the Vitamin D Receptor and Hairless Corepressor, Two Proteins Required for Hair Cycling
Vitamin D receptor and hairless protein are essential for hair growth.
research 17β-Estradiol Increases APE1/Ref-1 Secretion in Vascular Endothelial Cells and Ovariectomized Mice: Involvement of Calcium-Dependent Exosome Pathway
17β-estradiol boosts APE1/Ref-1 secretion in cells and mice via a calcium-dependent pathway.
research Dynamic regulation of retinoic acid-binding proteins in developing, adult and neoplastic skin reveals roles for β-catenin and Notch signalling
Retinoic acid-binding proteins in skin are regulated by β-catenin and Notch signalling.
research Epiregulin promotes hair growth via EGFR‐medicated epidermal and ErbB4‐mediated dermal stimulation
Epiregulin can help hair grow and may be useful for treating hair loss.
research Analysis of hairless corepressor mutants to characterize molecular cooperation with the vitamin D receptor in promoting the mammalian hair cycle
Certain mutations in the hairless protein disrupt its ability to regulate the hair cycle.
research Minireview: vitamin D receptor: new assignments for an already busy receptor. - eScholarship
The vitamin D receptor has many roles in the body beyond managing calcium, affecting the immune system, hair growth, muscles, fat, bone marrow, and cancer cells.
research Expression of retinoid nuclear receptor superfamily members in human hair follicles and its implication in hair growth.
RXR agonists may promote hair growth in humans.
research Data from Ribonucleotide Excision Repair Is Essential to Prevent Squamous Cell Carcinoma of the Skin
Ribonucleotide excision repair is crucial to prevent skin cancer.
research The Auxin-Regulated CrRLK1L Kinase ERULUS Controls Cell Wall Composition during Root Hair Tip Growth
ERULUS controls root hair growth by regulating cell wall composition and pectin activity.
research Pinkie, the First Viable Germline Hypomorph Allele of Retinoid X Receptor Alpha, Reveals an Important Role for RXRa in Th2 Development.
RXRa is crucial for Th2 immune cell development and may link nutrition to immune health.
research Retinoic Acid and Mouse Skin Morphogenesis. II. Role of Epidermal Competence in Hair Glandular Metaplasia
Retinoic acid causes gland formation instead of hair in mouse skin by altering epidermal and dermal interactions.
research Cellular localization of retinoic acid receptor-gamma expression in normal and neoplastic skin.
RAR-gamma 1 is important for normal skin maintenance and differentiation.
research Two Opposing Faces of Retinoic Acid: Induction of Stemness or Induction of Differentiation Depending on Cell-Type
Retinoic acid can either maintain stem cells or make them specialize, depending on the cell type.
research Data from Ribonucleotide Excision Repair Is Essential to Prevent Squamous Cell Carcinoma of the Skin
Ribonucleotide excision repair is crucial to prevent skin cancer.
research Modulation of Vitamin D Receptor Activity by the Corepressor Hairless: Differential Effects of Hairless Isoforms
Different Hairless isoforms affect Vitamin D receptor activity in hair regulation, with one repressing and the other stimulating it.
research Ribonucleotide Excision Repair Is Essential to Prevent Squamous Cell Carcinoma of the Skin
Fixing DNA errors is crucial to prevent skin cancer.
research Expression, characterization, and structural analysis of human liver delta4-3-ketosteroid 5beta-reductase (AKR1D1) and its disease-related mutant P133R
The P133R mutation in AKR1D1 enzyme causes harmful bile acid buildup, explaining related health issues.