research Stabilization of Epithelial Beta-Catenin Compromises Mammary Cell Fate Acquisition and Branching Morphogenesis
Keeping β-catenin levels high in mammary cells disrupts their development and branching.
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research Stabilization of Epithelial Beta-Catenin Compromises Mammary Cell Fate Acquisition and Branching Morphogenesis
Too much β-catenin activity can mess up the development of mammary glands and make them more like hair follicles.
research Genetic Basis of Skin Appendage Development
Hair, teeth, and mammary glands develop similarly at first but use different genes later.
research Sostdc1 Defines the Size and Number of Skin Appendage Placodes
Sostdc1 controls the size and number of hair and mammary gland structures.
research Early Inductive Events in Ectodermal Appendage Morphogenesis
Early development of hair, teeth, and glands involves specific signaling pathways and cellular interactions.
research Hedgehog And Gli Signaling In Embryonic Mammary Gland Development
Hedgehog signaling is crucial for mammary gland development over hair follicles.
research TNF Superfamily in Skin Appendage Development
TNF family proteins are crucial for the development of skin features like hair, teeth, and mammary glands.
research Neuregulin3 Alters Cell Fate in the Epidermis and Mammary Gland
Neuregulin3 affects cell development in the skin and mammary glands.
research Wnt Target Gene Ascl4 Is Dispensable for Skin Appendage Development
The gene Ascl4 is not necessary for the development of hair, teeth, or mammary glands.
research Specific Ectodermal Enhancers Control the Expression of Hoxc Genes in Developing Mammalian Integuments
The HoxC gene cluster and its enhancers are essential for developing hair and nails in mammals.
research WNT10A Mutation Causes Ectodermal Dysplasia by Impairing Progenitor Cell Proliferation and KLF4-Mediated Differentiation
A WNT10A gene mutation leads to ectodermal dysplasia by disrupting cell growth and differentiation.
research Hair Keratin KRT81 Is Expressed in Normal and Breast Cancer Cells and Contributes to Their Invasiveness
The hair keratin gene KRT81 is found in both normal and breast cancer cells and helps them invade surrounding tissues.
research Identification of Dkk4 as a Target of Eda-A1/Edar Pathway Reveals an Unexpected Role of Ectodysplasin as Inhibitor of Wnt Signaling in Ectodermal Placodes
Ectodysplasin inhibits Wnt signaling to help form hair follicles.
research Identification of Stem Cell Populations in Sweat Glands and Ducts Reveals Roles in Homeostasis and Wound Repair
The study found that sweat glands contain different types of stem cells that help with healing and maintaining healthy skin.
research Conversion of the Nipple to Hair-Bearing Epithelia by Lowering Bone Morphogenetic Protein Pathway Activity at the Dermal-Epidermal Interface
Blocking a specific protein signal can make hair grow on mouse nipples.
research Expression of Foxi3 Is Regulated by Ectodysplasin in Skin Appendage Placodes
Foxi3 expression in developing teeth and hair is controlled by the ectodysplasin pathway.
research The Mesenchymal Component of Hair Follicle Neogenesis: Background, Methods, and Molecular Characterization
The document concludes that specific cells are essential for hair growth and more research is needed to understand how to maintain their hair-inducing properties.
research Involvement of Wnt, Eda, and Shh at Defined Stages of Sweat Gland Development
Wnt, Eda, and Shh pathways are crucial for different stages of sweat gland development in mice.
research Induction of Hair Follicle Dermal Papilla Cell Properties in Human Induced Pluripotent Stem Cell-Derived Multipotent LNGFR(+)THY-1(+) Mesenchymal Cells
Researchers found a way to create cells from stem cells that act like human cells important for hair growth and could be used for hair regeneration treatments.
research Control by a Hair’s Breadth: The Role of MicroRNAs in the Skin
MicroRNAs play a crucial role in skin and hair health, affecting everything from growth to aging, and could potentially be used in treating skin diseases.
research Ectodysplasin Research: Where to Next?
Future research on ectodysplasin should explore its role in diseases, stem cells, and evolution, and continue developing treatments for genetic disorders like hypohidrotic ectodermal dysplasia.
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 Keratinocyte-Specific Ablation of the NF-κB Regulatory Protein A20 (TNFAIP3) Reveals a Role in the Control of Epidermal Homeostasis
A20 protein is crucial for normal skin and hair development.
research Hair-Cycle-Dependent Expression of Parathyroid Hormone-Related Protein and Its Type I Receptor: Evidence for Regulation at the Anagen to Catagen Transition
Parathyroid hormone-related protein helps control hair growth phases in mice.
research Identification of Ectodysplasin Target Genes Reveals the Involvement of Chemokines in Hair Development
Chemokine signaling is important for hair development.
research Genotype-Phenotype Correlation in Boys with X-Linked Hypohidrotic Ectodermal Dysplasia
Boys with less severe EDA mutations in XLHED have milder symptoms and better sweat and hair production.
research Harnessing Neuroendocrine Controls of Keratin Expression: A New Therapeutic Strategy for Skin Diseases?
Using neurohormones to control keratin can lead to new skin disease treatments.
research Rac-Dependent Signaling from Keratinocytes Promotes Differentiation of Intradermal White Adipocytes
Signals from skin cells controlled by Rac proteins help turn certain precursor cells into white fat cells.
research A Transient Dermal Niche and Dual Epidermal Programs Underlie Sweat Gland Development
Sweat gland development involves two unique skin cell programs and a temporary skin environment.
research Enhancement of Hair Growth Through Stimulation of Dermal Papilla Cells in Human Follicular Dermal
Biofield Energy Healing significantly increased hair growth by making hair root cells grow more.