ArticleThe Journal of cell biology1998
Activation of the MAP kinase pathway by FGF-1 correlates with cell proliferation induction while activation of the Src pathway correlates with migration.
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 43 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
43 citing papers in PubMed, 129 citations in OpenAlex.
- Functions of Epimedin C in a zebrafish model of glucocorticoid-induced osteoporosis.Journal of cellular and molecular medicine · 2024Article
- Increased c‑SRC expression is involved in acquired resistance to lenvatinib in hepatocellular carcinoma.Oncology letters · 2023Article
- Impact of FGF1 on human periodontal ligament fibroblast growth, osteogenic differentiation and inflammatory reaction in vitro.Journal of orofacial orthopedics = Fortschritte der Kieferorthopadie : Organ/official journal Deutsche Gesellschaft fur Kieferorthopadie · 2022Article
- TGF-β2 enhances expression of equine bone marrow-derived mesenchymal stem cell paracrine factors with known associations to tendon healing.Stem cell research & therapy · 2022Article
- CD40 Cross-Linking Induces Migration of Renal Tumor Cell through Nuclear Factor of Activated T Cells (NFAT) Activation.International journal of molecular sciences · 2021Article
- Review
- Acidic fibroblast growth factor underlies microenvironmental regulation of MYC in pancreatic cancer.The Journal of experimental medicine · 2020Article
- Stable Fibroblast Growth Factor 2 Dimers with High Pro-Survival and Mitogenic Potential.International journal of molecular sciences · 2020Article
- Review
- FGFR- gene family alterations in low-grade neuroepithelial tumors.Acta neuropathologica communications · 2020Review
- Resistance to Anti-angiogenic Therapies: A Mechanism Depending on the Time of Exposure to the Drugs.Frontiers in cell and developmental biology · 2020Review
- Resistance Mechanisms to Anti-angiogenic Therapies in Cancer.Frontiers in oncology · 2020Review
- The Role of FGF9 in the Production of Neural Retina and RPE in a Pluripotent Stem Cell Model of Early Human Retinal Development.American journal of ophthalmology · 2019Article
- Article
- Resistance to Anti-Angiogenic Therapy in Cancer-Alterations to Anti-VEGF Pathway.International journal of molecular sciences · 2018Review
- Inhibition of the fibroblast growth factor receptor (FGFR) pathway: the current landscape and barriers to clinical application.Oncotarget · 2017Review
- Evaluation of the efficacy of dasatinib, a Src/Abl inhibitor, in colorectal cancer cell lines and explant mouse model.PloS one · 2017Article
- ZDHHC3 Tyrosine Phosphorylation Regulates Neural Cell Adhesion Molecule Palmitoylation.Molecular and cellular biology · 2016Article
- Slit2/Robo1 signaling promotes intestinal tumorigenesis through Src-mediated activation of the Wnt/β-catenin pathway.Oncotarget · 2015Article
- Copper binding affinity of the C2B domain of synaptotagmin-1 and its potential role in the nonclassical secretion of acidic fibroblast growth factor.Biochimica et biophysica acta · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
FGF regulates both cell migration and proliferation by receptor-dependent induction of immediate-early gene expression and tyrosine phosphorylation of intracellular polypeptides. Because little is known about the disparate nature of intracellular signaling pathways, which are able to discriminate between cell migration and proliferation, we used a washout strategy to examine the relationship between immediate-early gene expression and tyrosine phosphorylation with respect to the potential of cells either to migrate or to initiate DNA synthesis in response to FGF-1. We demonstrate that transient exposure to FGF-1 results in a significant decrease in Fos transcript expression and a decrease in tyrosine phosphorylation of the FGFR-1, p42(mapk), and p44(mapk). Consistent with these biochemical effects, we demonstrate that attenuation in the level of DNA synthesis such that a 1.5-h withdrawal is sufficient to return the population to a state similar to quiescence. In contrast, the level of Myc mRNA, the activity of Src, the tyrosine phosphorylation of cortactin, and the FGF-1-induced redistribution of cortactin and F-actin were unaffected by transient FGF-1 stimulation. These biochemical responses are consistent with an implied uncompromised migratory potential of the cells in response to growth factor withdrawal. These results suggest a correlation between Fos expression and the mitogen-activated protein kinase pathway with initiation of DNA synthesis and a correlation between high levels of Myc mRNA and Src kinase activity with the regulation of cell migration.
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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.