ArticleJournal of cell science2006
Dystroglycan loss disrupts polarity and beta-casein induction in mammary epithelial cells by perturbing laminin anchoring.
Article in Journal of cell science, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
58 citing papers in PubMed, 27 citations in OpenAlex.
- Mechanisms of Regulation of Cell Fate in Breast Development and Cancer.Advances in experimental medicine and biology · 2025Review
- Suppression of dystroglycan function accompanies pancreatic acinar-to-ductal metaplasia and favours dysplasia development.The Journal of pathology · 2024Article
- Involvement of abnormal dystroglycan expression and matriglycan levels in cancer pathogenesis.Cancer cell international · 2022Review
- The Mammary Gland: Basic Structure and Molecular Signaling during Development.International journal of molecular sciences · 2022Review
- The Role of Extracellular Matrix Proteins in Breast Cancer.Journal of clinical medicine · 2022Review
- Abnormal promoter DNA hypermethylation of the integrin, nidogen, and dystroglycan genes in breast cancer.Scientific reports · 2021Article
- Generating a Fractal Microstructure of Laminin-111 to Signal to Cells.Journal of visualized experiments : JoVE · 2020Article
- Oriented basement membrane fibrils provide a memory for F-actin planar polarization via the Dystrophin-Dystroglycan complex during tissue elongation.Development (Cambridge, England) · 2020Article
- Proteomic Analysis of Urinary Extracellular Vesicles Reveals a Role for the Complement System in Medullary Sponge Kidney Disease.International journal of molecular sciences · 2019Article
- The microstructure of laminin-111 compensates for dystroglycan loss in mammary epithelial cells in downstream expression of milk proteins.Biomaterials · 2019Article
- Assembly of the β4-Integrin Interactome Based on Proximal Biotinylation in the Presence and Absence of Heterodimerization.Molecular & cellular proteomics : MCP · 2019Article
- Article
- Dystroglycan Suppresses Notch to Regulate Stem Cell Niche Structure and Function in the Developing Postnatal Subventricular Zone.Developmental cell · 2016Article
- Human mesenchymal stem cell response to poly(ε-caprolactone/poly(methyl methacrylate) demixed thin films.Journal of materials science. Materials in medicine · 2015Article
- Metastasis prevention by targeting the dormant niche.Nature reviews. Cancer · 2015Review
- Phosphoinositide 3-kinase p110δ promotes lumen formation through the enhancement of apico-basal polarity and basal membrane organization.Nature communications · 2015Article
- Endocytic trafficking of laminin is controlled by dystroglycan and is disrupted in cancers.Journal of cell science · 2014Article
- Integrins and epithelial cell polarity.Journal of cell science · 2014Review
- Phosphorylation of the E3 ubiquitin ligase RNF41 by the kinase Par-1b is required for epithelial cell polarity.Journal of cell science · 2014Article
- Extracellular matrix proteins regulate epithelial-mesenchymal transition in mammary epithelial cells.Differentiation; research in biological diversity · 2013Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Precise contact between epithelial cells and their underlying basement membrane is crucial to the maintenance of tissue architecture and function. To understand the role that the laminin receptor dystroglycan (DG) plays in these processes, we assayed cell responses to laminin-111 following conditional ablation of DG gene (Dag1) expression in cultured mammary epithelial cells. Strikingly, DG loss disrupted laminin-111-induced polarity and beta-casein production, and abolished laminin assembly at the step of laminin binding to the cell surface. Dystroglycan re-expression restored these deficiencies. Investigations of the mechanism revealed that DG cytoplasmic sequences were not necessary for laminin assembly and signaling, and only when the entire mucin domain of extracellular DG was deleted did laminin assembly not occur. These results demonstrate that DG is essential as a laminin-111 co-receptor in mammary epithelial cells that functions by mediating laminin anchoring to the cell surface, a process that allows laminin polymerization, tissue polarity and beta-casein induction. The observed loss of laminin-111 assembly and signaling in Dag1(-/-) mammary epithelial cells provides insights into the signaling changes occurring in breast carcinomas and other cancers, where the binding function of DG to laminin is frequently defective.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.