ArticleThe Journal of cell biology2002
N-cadherin-dependent cell-cell contact regulates Rho GTPases and beta-catenin localization in mouse C2C12 myoblasts.
Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 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
109 citing papers in PubMed, 226 citations in OpenAlex.
- Electrical stimulation promotes structural plasticity in cortical spheroids by modulating N-cadherin-dependent collective migration and mechanotransduction.Biomedical engineering letters · 2026Article
- Single-cell transcriptomics reveal mechanisms of skeletal muscle differentiation across duck embryonic development.Communications biology · 2026Article
- Article
- Unresolved mechanisms: a hypothesized spatial regulation of myosin light chain phosphorylation within the walls of resistance arteries.Frontiers in physiology · 2026Article
- Vitamin B1 Involved inInternational journal of molecular sciences · 2025Article
- CAR links hypoxia signaling to improved survival after myocardial infarction.Experimental & molecular medicine · 2023Article
- Chondroitin sulfate E downregulates N-cadherin and suppresses myotube formation.The Journal of veterinary medical science · 2022Article
- Fusion of Normoxic- and Hypoxic-Preconditioned Myoblasts Leads to Increased Hypertrophy.Cells · 2022Article
- Delta-Catenin as a Modulator of Rho GTPases in Neurons.Frontiers in cellular neuroscience · 2022Review
- Condensation tendency and planar isotropic actin gradient induce radial alignment in confined monolayers.eLife · 2021Article
- Stochastic Dynamics of Gene Switching and Energy Dissipation for Gene Expression.Frontiers in genetics · 2020Article
- DEPDC1B is a key regulator of myoblast proliferation in mouse and man.Cell proliferation · 2020Article
- Molecular Mechanisms of Cadherin Function During Cortical Migration.Frontiers in cell and developmental biology · 2020Review
- Directed Collective Cell Migration Using Three-Dimensional Bioprinted Micropatterns on Thermoresponsive Surfaces for Myotube Formation.ACS biomaterials science & engineering · 2019Article
- Discoidin domain receptor 1 deficiency in vascular smooth muscle cells leads to mislocalisation of N-cadherin contacts.Biology open · 2019Article
- N-cadherin signaling via Trio assembles adherens junctions to restrict endothelial permeability.The Journal of cell biology · 2019Article
- The Trithorax protein Ash1L promotes myoblast fusion by activating Cdon expression.Nature communications · 2018Article
- Spatiotemporal regulation of the GPCR activity of BAI3 by C1qL4 and Stabilin-2 controls myoblast fusion.Nature communications · 2018Article
- N-cadherin in cancer metastasis, its emerging role in haematological malignancies and potential as a therapeutic target in cancer.BMC cancer · 2018Review
- COMP-Angiopoietin-1 accelerates muscle regeneration through N-cadherin activation.Scientific reports · 2018Article
49 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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-cadherin, a member of the Ca(2+)-dependent cell-cell adhesion molecule family, plays an essential role in skeletal muscle cell differentiation. We show that inhibition of N-cadherin-dependent adhesion impairs the upregulation of the two cyclin-dependent kinase inhibitors p21 and p27, the expression of the muscle-specific genes myogenin and troponin T, and C2C12 myoblast fusion. To determine the nature of N-cadherin-mediated signals involved in myogenesis, we investigated whether N-cadherin-dependent adhesion regulates the activity of Rac1, Cdc42Hs, and RhoA. N-cadherin-dependent adhesion decreases Rac1 and Cdc42Hs activity, and as a consequence, c-jun NH2-terminal kinase (JNK) MAPK activity but not that of the p38 MAPK pathway. On the other hand, N-cadherin-mediated adhesion increases RhoA activity and activates three skeletal muscle-specific promoters. Furthermore, RhoA activity is required for beta-catenin accumulation at cell-cell contact sites. We propose that cell-cell contacts formed via N-cadherin trigger signaling events that promote the commitment to myogenesis through the positive regulation of RhoA and negative regulation of Rac1, Cdc42Hs, and JNK activities.
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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.