ArticleCell stem cell2019
EGFR-Aurka Signaling Rescues Polarity and Regeneration Defects in Dystrophin-Deficient Muscle Stem Cells by Increasing Asymmetric Divisions.
Article in Cell stem cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 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
87 citing papers in PubMed, 147 citations in OpenAlex.
- CRISPR-Enabled functional genomics in hPSCs-derived neural models for autism spectrum disorder.Metabolic brain disease · 2026Review
- Duchenne muscular dystrophy: from gene to gene-ius therapies.Skeletal muscle · 2026Review
- Stimulation of EGFR signaling in fibro-adipogenic precursors decreases adipogenesis in Duchenne muscular dystrophy.Skeletal muscle · 2026Article
- Activating FGFR1 restores Integrin-β1-mediated fibronectin sensing in satellite cells of aged mice.bioRxiv : the preprint server for biology · 2026Article
- Impaired stem cell migration and divisions in Duchenne muscular dystrophy revealed by live imaging.Nature communications · 2026Article
- Investigating the role of EGFR signalling in muscle dystrophies: implications for Duchenne muscular dystrophy.Cell death & disease · 2026Article
- Lineage relationships in muscle stem cells: linking functional fate to molecular state.Frontiers in cell and developmental biology · 2026Review
- Proximity Ligation Assay to Determine Protein-Protein Interactions in Muscle Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Conditional Dmd ablation in muscle and brain causes profound effects on muscle function and neurobehavior.Communications biology · 2025Article
- Loss of cell-autonomously secreted laminin-α2 drives muscle stem cell dysfunction in LAMA2-related muscular dystrophy.Nature communications · 2025Article
- TGFβ-Smad3 signaling restores cell-autonomous Srsf1-mediated splicing of fibronectin in aged skeletal muscle stem cells.Nature communications · 2025Article
- Translational progress in the development of pharmacotherapies for Duchenne muscular dystrophy.Regenerative medicine · 2025Article
- Regulatory Landscapes of Muscle Satellite Cells: From Mechanism to Application.International journal of stem cells · 2025Review
- Enrichment of ornithine decarboxylase degron transduced colorectal cancer cells for extended application of cancer stem cell models.Scientific reports · 2025Article
- Article
- Single-nucleus transcriptomics reveals subsets of degenerative myonuclei after rotator cuff tear-induced muscle atrophy.Cell proliferation · 2025Article
- Intrinsic Muscle Stem Cell Dysfunction Contributes to Impaired Regeneration in the mdx Mouse.Journal of cachexia, sarcopenia and muscle · 2025Article
- Succinate Regulates Exercise-Induced Muscle Remodelling by Boosting Satellite Cell Differentiation Through Succinate Receptor 1.Journal of cachexia, sarcopenia and muscle · 2025Article
- Aptamer-conjugated gold nanoparticles enable oligonucleotide delivery into muscle stem cells to promote regeneration of dystrophic muscles.Nature communications · 2025Article
- PTPN1/2 inhibition promotes muscle stem cell differentiation in Duchenne muscular dystrophy.Life science alliance · 2025Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Loss of dystrophin expression in Duchenne muscular dystrophy (DMD) causes progressive degeneration of skeletal muscle, which is exacerbated by reduced self-renewing asymmetric divisions of muscle satellite cells. This, in turn, affects the production of myogenic precursors and impairs regeneration and suggests that increasing such divisions may be beneficial. Here, through a small-molecule screen, we identified epidermal growth factor receptor (EGFR) and Aurora kinase A (Aurka) as regulators of asymmetric satellite cell divisions. Inhibiting EGFR causes a substantial shift from asymmetric to symmetric division modes, whereas EGF treatment increases asymmetric divisions. EGFR activation acts through Aurka to orient mitotic centrosomes, and inhibiting Aurka blocks EGF stimulation-induced asymmetric division. In vivo EGF treatment markedly activates asymmetric divisions of dystrophin-deficient satellite cells in mdx mice, increasing progenitor numbers, enhancing regeneration, and restoring muscle strength. Therefore, activating an EGFR-dependent polarity pathway promotes functional rescue of dystrophin-deficient satellite cells and enhances muscle force generation.
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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.