ArticleMatrix biology : journal of the International Society for Matrix Biology2009
Regulation of p38 MAP kinase by anastellin is independent of anastellin's effect on matrix fibronectin.
Article in Matrix biology : journal of the International Society for Matrix Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Anastellin: A Fibronectin-Derived Peptide Targeting the Tumor Microenvironment Through ECM Modulation.Cell biochemistry and biophysics · 2026Review
- Anastellin impacts on the processing of extracellular matrix fibronectin and stimulates release of cytokines from coronary artery smooth muscle cells.Scientific reports · 2022Article
- Tumor Microenvironment: Extracellular Matrix Alterations Influence Tumor Progression.Frontiers in oncology · 2020Review
- The Effects of a Novel Series of KTTKS Analogues on Cytotoxicity and Proteolytic Activity.Molecules (Basel, Switzerland) · 2019Article
- Chlorination and oxidation of human plasma fibronectin by myeloperoxidase-derived oxidants, and its consequences for smooth muscle cell function.Redox biology · 2018Article
- Vasoactive effect of fibronectin-derived epiviosamine-1 and related peptides in quiescent and stress models.Microcirculation (New York, N.Y. : 1994) · 2017Article
- Conformational remodeling of the fibronectin matrix selectively regulates VEGF signaling.Journal of cell science · 2014Article
- Regulation of the innate immune response by fibronectin: synergism between the III-1 and EDA domains.PloS one · 2014Article
- The first type III repeat in fibronectin activates an inflammatory pathway in dermal fibroblasts.The Journal of biological chemistry · 2010Article
- Endostatin and anastellin inhibit distinct aspects of the angiogenic process.Journal of experimental & clinical cancer research : CR · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Anastellin is an angiogenesis inhibitor derived from the first type III repeat of fibronectin (FN). Anastellin binds to fibronectin and promotes the polymerization of soluble fibronectin into a highly polymerized form termed superfibronectin. In addition, anastellin also causes remodeling of pre-existing fibronectin matrix and modulates cell signaling pathways in both endothelial cells and fibroblasts. In the present study, we address the relationship of anastellin's effects on fibronectin matrix to its effects on p38 MAP kinase (MAPK) activation. Using a mutant form of anastellin which binds to fibronectin matrix, but does not stimulate formation of superfibronectin, we demonstrate that the activation of p38 MAPK by anastellin is not dependent on the formation of superfibronectin. The mutant form of anastellin does stimulate matrix remodeling, but experiments using FN(-/-) cells show that the effect of anastellin on p38-MAPK activation is completely independent of fibronectin. Anastellin was able to activate p38 MAPK on cells in suspension as well as on cells null for beta1 integrins, suggesting that anastellin activity did not require ligation of integrins. These data suggest that the activation of p38 MAPK by anastellin is independent of anastellin's effects on fibronectin matrix organization.
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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.