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Characterization of E-Cadherin, SSEA-1, MSI-1, and SOX-2 Expression and Their Association with Pale Cells in Adenomyosis.
Biomolecules
October 2024
Department of Gynecology and Obstetrics, Münster University Hospital, Labor PAN-Zentrum, Vesaliusweg 2-4, 48149 Münster, Germany.
Article Synopsis
- Adenomyosis (AM) is a reproductive health condition where endometrial tissue grows into the uterine muscle, but its causes and development are not fully understood.
- A new type of cell, called pale cells, has been discovered; these cells lack certain connections and are seen moving through tiny breaks in the tissue, suggesting they may have unique properties.
- The research analyzed 40 hysterectomy samples to check for specific stem cell markers, finding that pale cells often expressed a stem cell marker called SSEA-1, hinting that these cells could play a role in the development of adenomyosis, and more research is needed to explore this further.
Study repair function of mucin-2 on the tight junction protein of uterine epithelial cells under bacterial endotoxins.
Toxicon
December 2024
College of Animal Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, 712100, China. Electronic address:
To analysis repair function of mucin-2(MUC2) and glycoprotein particles on the tight junction protein of uterus under bacterial endotoxins. In this experiment, we showed that the thicker mucus layer of the uterus is used to prevent the translocation of endotoxin at 21d postdelivery. When endotoxin acts on the uterus to thin its mucous layer, the cells in the lamina propria of the uterus secrete a large number of glycoprotein particles at 27d postdelivery.
View Article and Find Full Text PDFThe transmembrane domain of the desmosomal cadherin desmoglein-1 governs lipid raft association to promote desmosome adhesive strength.
Mol Biol Cell
December 2024
Departments of Dermatology and Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, PA 17033.
Article Synopsis
- Lipid rafts are specialized areas in cell membranes that help organize proteins and regulate cellular functions, but how desmosomal proteins interact with these rafts is not well understood.
- Researchers focused on desmoglein-1 (DSG1), a key desmosomal protein, and found that specific features of its transmembrane domain (TMD), such as length and size, significantly affect its association with lipid rafts.
- The study concluded that the efficient association of DSG1 with lipid rafts is crucial for the formation and stability of desmosomes, which are important for cell adhesion and mechanical strength.
Binding to the neonatal Fc receptor enhances the pathogenicity of anti-desmoglein-3 antibodies in keratinocytes.
Front Immunol
October 2024
Institute of Biochemistry, Medical Faculty, University of Giessen, Giessen, Germany.
The neonatal Fc receptor (FcRn) is important for numerous cellular processes that involve antibody recycling and trafficking. A major function of FcRn is IgG recycling and half-life prolongation, and FcRn blockade results in a reduction of autoantibodies in IgG-mediated autoimmune diseases. In epithelial cells, FcRn functions in processes different from IgG recycling, such as antibody transcytosis in intestinal cells.
View Article and Find Full Text PDFUpregulation of keratin 15 is required for varicella-zoster virus replication in keratinocytes and is attenuated in the live attenuated vOka vaccine strain.
Virol J
October 2024
Infection, Immunity and Inflammation Department, University College London GOS Institute of Child Health, London, UK.
Varicella-zoster virus (VZV) is the etiological agent of chickenpox and shingles, diseases characterised by epidermal virus replication in skin and mucosa and the formation of blisters. We have previously shown that VZV infection has a profound effect on keratinocyte differentiation, altering the normal pattern of epidermal gene expression. In particular, VZV infection reduces expression of suprabasal keratins 1 and 10 and desmosomal proteins, disrupting epidermal structure to promote expression of a blistering phenotype.
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