ArticleCell reports2017
Niche Cadherins Control the Quiescence-to-Activation Transition in Muscle Stem Cells.
Article in Cell reports, 2017. 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, 142 citations in OpenAlex.
- Integrating and Orchestrating Multiple Components of Skeletal Muscle Injury and Regeneration.American journal of physiology. Cell physiology · 2026Article
- Androgen receptor imprints satellite cell stemness and preserves their reservoir for lifelong regeneration and optimal repair.Science advances · 2026Article
- GDF5 modulation of MuSC pool as a potential therapeutic benefit for DMD.Molecular therapy. Nucleic acids · 2026Article
- State-Dependent FGF Signaling in Satellite Cell-Mediated Skeletal Muscle Regeneration and Pathological Remodeling.Biomolecules · 2026Review
- Exercise, Prostaglandin ECells · 2026Review
- Mechanical Signaling Regulates DNA Methylation to Maintain Muscle Stem Cell Quiescence.bioRxiv : the preprint server for biology · 2026Article
- Mechanobiological landscape of muscle stem cells.Skeletal muscle · 2026Review
- Prostaglandin E2 receptor EP2 is indispensable for maintenance of skeletal muscle stem cells.Stem cells (Dayton, Ohio) · 2026Article
- M-cadherin regulates the formation of adherens junctions and secondary myofibers during fetal myogenesis to determine adult myofiber number and muscle mass.Stem cell reports · 2026Article
- Development of a split-toxin CRISPR screening platform to systematically identify regulators of human myoblast fusion.Nature communications · 2026Article
- Non-regenerative myogenesis in adult skeletal muscles: myofiber death-independent muscle satellite cell expansion.Skeletal muscle · 2026Review
- Planar cell polarity protein Vangl2 interacts with M-cadherin and stabilizes its cell surface expression in mouse C2C12 myoblasts.Frontiers in cell and developmental biology · 2026Article
- Musculoskeletal ultrasound-guided cellular therapy: Current applications and future directions in skeletal muscle regeneration.Iranian journal of basic medical sciences · 2026Review
- Transdifferentiation of endothelial progenitor cells into rhabdomyosarcoma defined by hedgehog signaling competence.Cell reports · 2025Article
- Development of an anti-CDH15/M-cadherin monoclonal antibody CaBiochemistry and biophysics reports · 2025Article
- The glycosyltransferase POGLUT1 regulates muscle stem cell development and maintenance in mice.PLoS genetics · 2025Article
- Quiescence Multiverse.Biomolecules · 2025Review
- 3D Mechanical Confinement Directs Muscle Stem Cell Fate and Function.Advanced biology · 2025Article
- Mechanotransductive N-cadherin binding induces differentiation in human neural stem cells.Mechanobiology in medicine · 2025Article
- Myofibers cultured in viscoelastic hydrogels reveal the effects of integrin-binding and mechanosensing on muscle satellite cells.Acta biomaterialia · 2025Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Many adult stem cells display prolonged quiescence, promoted by cues from their niche. Upon tissue damage, a coordinated transition to the activated state is required because non-physiological breaks in quiescence often lead to stem cell depletion and impaired regeneration. Here, we identify cadherin-mediated adhesion and signaling between muscle stem cells (satellite cells [SCs]) and their myofiber niche as a mechanism that orchestrates the quiescence-to-activation transition. Conditional removal of N-cadherin and M-cadherin in mice leads to a break in SC quiescence, with long-term expansion of a regeneration-proficient SC pool. These SCs have an incomplete disruption of the myofiber-SC adhesive junction and maintain niche residence and cell polarity, yet show properties of SCs in a state of transition from quiescence toward full activation. Among these is nuclear localization of β-catenin, which is necessary for this phenotype. Injury-induced perturbation of niche adhesive junctions is therefore a likely first step in the quiescence-to-activation transition.
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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.