ArticleThe Journal of cell biology2000
Tenascin-C suppresses Rho activation.
Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.
- Systematic review of protein biomarkers of invasive behavior in glioblastoma.Molecular neurobiology · 2014Pooled it
- Shaping Oncogenic Microenvironments: Contribution of Fibronectin.Frontiers in cell and developmental biology · 2024Review
- The coordinated activities of collagen VI and XII in maintenance of tissue structure, function and repair: evidence for a physical interaction.Frontiers in molecular biosciences · 2024Article
- Biology of Tenascin C and its Role in Physiology and Pathology.Current medicinal chemistry · 2024Review
- Article
- Targeting the cytoskeleton and extracellular matrix in cardiovascular disease drug discovery.Expert opinion on drug discovery · 2022Review
- Tumor Cell Infiltration into the Brain in Glioblastoma: From Mechanisms to Clinical Perspectives.Cancers · 2022Review
- Revisiting the Tenascins: Exploitable as Cancer Targets?Frontiers in oncology · 2022Review
- Tenascins Interfere With Remyelination in an Ex Vivo Cerebellar Explant Model of Demyelination.Frontiers in cell and developmental biology · 2022Article
- Tension Stimulation of Tenocytes in Aligned Hyaluronic Acid/Platelet-Rich Plasma-Polycaprolactone Core-Sheath Nanofiber Membrane Scaffold for Tendon Tissue Engineering.International journal of molecular sciences · 2021Article
- Differential cellular responses to adhesive interactions with galectin-8- and fibronectin-coated substrates.Journal of cell science · 2021Article
- Autophagy deficiency promotes triple-negative breast cancer resistance to T cell-mediated cytotoxicity by blocking tenascin-C degradation.Nature communications · 2020Article
- The Cytoskeleton-A Complex Interacting Meshwork.Cells · 2019Review
- Counterbalancing anti-adhesive effects of Tenascin-C through fibronectin expression in endothelial cells.Scientific reports · 2017Article
- Tenascin C in metastasis: A view from the invasive front.Cell adhesion & migration · 2015Review
- Tenascin-C-derived peptide TNIIIA2 highly enhances cell survival and platelet-derived growth factor (PDGF)-dependent cell proliferation through potentiated and sustained activation of integrin α5β1.The Journal of biological chemistry · 2014Article
- Insidious changes in stromal matrix fuel cancer progression.Molecular cancer research : MCR · 2014Review
- Matrikine and matricellular regulators of EGF receptor signaling on cancer cell migration and invasion.Laboratory investigation; a journal of technical methods and pathology · 2014Review
- Three-dimensional culture environment increases the efficacy of platelet rich plasma releasate in prompting skin fibroblast differentiation and extracellular matrix formation.International journal of medical sciences · 2014Article
- Influence of cartilage extracellular matrix molecules on cell phenotype and neocartilage formation.Tissue engineering. Part A · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell binding to extracellular matrix (ECM) components changes cytoskeletal organization by the activation of Rho family GTPases. Tenascin-C, a developmentally regulated matrix protein, modulates cellular responses to other matrix proteins, such as fibronectin (FN). Here, we report that tenascin-C markedly altered cell phenotype on a three-dimensional fibrin matrix containing FN, resulting in suppression of actin stress fibers and induction of actin-rich filopodia. This distinct morphology was associated with complete suppression of the activation of RhoA, a small GTPase that induces actin stress fiber formation. Enforced activation of RhoA circumvented the effects of tenascin. Effects of active Rho were reversed by a Rho inhibitor C3 transferase. Suppression of GTPase activation allows tenascin-C expression to act as a regulatory switch to reverse the effects of adhesive proteins on Rho function. This represents a novel paradigm for the regulation of cytoskeletal organization by ECM.
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What OpenQuestion holds
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.