ArticleThe Journal of cell biology1998
Fibronectin matrix regulates activation of RHO and CDC42 GTPases and cell cycle progression.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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.
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
66 citing papers in PubMed, 230 citations in OpenAlex.
- Anastellin impacts on the processing of extracellular matrix fibronectin and stimulates release of cytokines from coronary artery smooth muscle cells.Scientific reports · 2022Article
- Peptides for Coating TiOInternational journal of molecular sciences · 2022Article
- Regulatory roles of fibronectin and integrin α5 in reorganization of the actin cytoskeleton and completion of adipogenesis.Molecular biology of the cell · 2022Article
- Review of Integrin-Targeting Biomaterials in Tissue Engineering.Advanced healthcare materials · 2020Review
- Article
- Fibrinogen Protects Against Barrier Dysfunction Through Maintaining Cell Surface Syndecan-1 In Vitro.Shock (Augusta, Ga.) · 2019Article
- Tumor-stromal crosstalk in pancreatic cancer and tissue fibrosis.Molecular cancer · 2019Review
- Impact of Interferon-α Receptor-1 Promoter Polymorphisms on the Transcriptome of the Hepatitis B Virus-Associated Hepatocellular Carcinoma.Frontiers in immunology · 2018Article
- Tumstatin regulates the angiogenic and inflammatory potential of airway smooth muscle extracellular matrix.Journal of cellular and molecular medicine · 2017Article
- Identification of novel Ack1-interacting proteins and Ack1 phosphorylated sites in mouse brain by mass spectrometry.Oncotarget · 2017Article
- Opposing FlnA and FlnB interactions regulate RhoA activation in guiding dynamic actin stress fiber formation and cell spreading.Human molecular genetics · 2017Article
- Matrix control of pancreatic cancer: New insights into fibronectin signaling.Cancer letters · 2016Review
- ARHGAP10, downregulated in ovarian cancer, suppresses tumorigenicity of ovarian cancer cells.Cell death & disease · 2016Article
- Cooperative effects of fibronectin matrix assembly and initial cell-substrate adhesion strength in cellular self-assembly.Acta biomaterialia · 2016Article
- Photocrosslinkable Gelatin Hydrogel for Epidermal Tissue Engineering.Advanced healthcare materials · 2016Article
- Rho GTPases as pathogen targets: Focus on curable sexually transmitted infections.Small GTPases · 2015Review
- Fibronectin matrix assembly is essential for cell condensation during chondrogenesis.Journal of cell science · 2014Article
- Bone regeneration using an alpha 2 beta 1 integrin-specific hydrogel as a BMP-2 delivery vehicle.Biomaterials · 2014Article
- Fibronectin matrix polymerization regulates smooth muscle cell phenotype through a Rac1 dependent mechanism.PloS one · 2014Article
- Extracellular matrix modulates angiogenesis in physiological and pathological conditions.BioMed research international · 2014Review
6 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 2 institutions in 4 countries.
Funding
Abstract
Adherent cells assemble fibronectin into a fibrillar matrix on their apical surface. The fibril formation is initiated by fibronectin binding to the integrins alpha5 beta1 and alphav beta3, and is completed by a process that includes fibronectin self-assembly. We found that a 76- amino acid fragment of fibronectin (III1-C) that forms one of the self-assembly sites caused disassembly of preformed fibronectin matrix without affecting cell adhesion. Treating attached fibroblasts or endothelial cells with III1-C inhibited cell migration and proliferation. Rho-dependent stress fiber formation and Rho-dependent focal contact protein phosphorylation were also inhibited, whereas Cdc42 was activated, leading to actin polymerization into filopodia. ACK (activated Cdc42-binding kinase) and p38 MAPK (mitogen-activated protein kinase), two downstream effectors of Cdc42, were activated, whereas PAK (p21-activated kinase) and JNK/SAPK (c-Jun NH2-terminal kinase/ stress-activated protein kinase) were inhibited. III1-C treatment also modulated activation of JNK and ERK (extracellular signal-regulated kinases) in response to growth factors, and reduced the activity of the cyclin E-cdk2 complex. These results indicate that the absence of fibronectin matrix causes activation of Cdc42, and that fibronectin matrix is required for Rho activation and cell cycle progression.
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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.