ArticleThe Journal of biological chemistry2012
Fibronectin induces endothelial cell migration through β1 integrin and Src-dependent phosphorylation of fibroblast growth factor receptor-1 at tyrosines 653/654 and 766.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 104 citations in OpenAlex.
- Fibronectin mediates APOE4-driven blood-brain barrier dysfunction in Alzheimer's disease.Nature aging · 2026Article
- Glycosylated Fibronectin in Fetal Growth Restriction: An Emerging Biomarker of Placental Dysfunction.Cureus · 2026Review
- Proteome-Wide Analysis of Functional Phosphosites in the FGFR Family of Proteins: Insights from Large-Scale Phosphoproteomic Analysis.Proteomes · 2026Article
- Interleukin-8 Overexpressing Collagen Microgel-Based Cellular Microtissue Accelerates the Healing of Diabetic Foot Ulcers.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- The impact of a high fat diet and platelet activation on pre-metastatic niche formation.Nature communications · 2025Article
- Fibronectin Mediates Endothelial-to-Mesenchymal Transition in Retina Angiogenesis.Investigative ophthalmology & visual science · 2025Article
- Mindin regulates fibroblast subpopulations through distinct Src family kinases during fibrogenesis.JCI insight · 2024Article
- Primitive macrophages enable long-term vascularization of human heart-on-a-chip platforms.Cell stem cell · 2024Article
- Secretome of Cancer-Associated Fibroblasts (CAFs) Influences Drug Sensitivity in Cancer Cells.Journal of proteome research · 2024Article
- Rare genetic variation in fibronectin 1 (FN1) protects against APOEε4 in Alzheimer's disease.Acta neuropathologica · 2024Article
- Differences in Genomic Alterations and Accumulations of Heavy Metals Between Advanced Non-small Cell Lung Cancer Patients with and without Bone Metastasis.Journal of Cancer · 2024Article
- PhysiMeSS - a new physiCell addon for extracellular matrix modelling.GigaByte (Hong Kong, China) · 2024Article
- Phosphoproteomic Changes Induced by Cell-Derived Matrix and Their Effect on Tumor Cell Migration and Cytoskeleton Remodeling.ACS biomaterials science & engineering · 2023Article
- Fibronectin fragments generated by pancreatic trypsin act as endogenous inhibitors of pancreatic tumor growth.Journal of experimental & clinical cancer research : CR · 2023Article
- The matricellular protein CCN3 supports lung endothelial homeostasis and function.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- A novel small molecule RK-019 inhibitsFrontiers in pharmacology · 2022Article
- Article
- Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling.Cells · 2021Review
- FN-EDA mediates angiogenesis of hepatic fibrosis via integrin-VEGFR2 in a CD63 synergetic manner.Cell death discovery · 2020Article
- CD99-PTPN12 Axis Suppresses Actin Cytoskeleton-Mediated Dimerization of Epidermal Growth Factor Receptor.Cancers · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The extracellular matrix microenvironment regulates cell phenotype and function. One mechanism by which this is achieved is the transactivation of receptor tyrosine kinases by specific matrix molecules. Here, we demonstrate that the provisional matrix protein, fibronectin (FN), activates fibroblast growth factor (FGF) receptor-1 (FGFR1) independent of FGF ligand in liver endothelial cells. FN activation of FGFR1 requires β1 integrin, as evidenced by neutralizing antibody and siRNA-based studies. Complementary genetic and pharmacologic approaches identify that the non-receptor tyrosine kinase Src is required for FN transactivation of FGFR1. Whereas FGF ligand-induced phosphorylation of FGFR1 preferentially activates ERK, FN-induced phosphorylation of FGFR1 preferentially activates AKT, indicating differential downstream signaling of FGFR1 in response to alternate stimuli. Mutation analysis of known tyrosine residues of FGFR1 reveals that tyrosine 653/654 and 766 residues are required for FN-FGFR1 activation of AKT and chemotaxis. Thus, our study mechanistically dissects a new signaling pathway by which FN achieves endothelial cell chemotaxis, demonstrates how differential phosphorylation profiles of FGFR1 can achieve alternate downstream signals, and, more broadly, highlights the diversity of mechanisms by which the extracellular matrix microenvironment regulates cell behavior through transactivation of receptor tyrosine kinases.
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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 Socratic graph.