ArticleProceedings of the National Academy of Sciences of the United States of America1999
Comparison of the intracellular signaling responses by three chimeric fibroblast growth factor receptors in PC12 cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 78 citations in OpenAlex.
- Targeting the cancer cells and cancer-associated fibroblasts with next-generation FGFR inhibitors in prostate cancer co-culture models.Cancer medicine · 2024Article
- Role of signaling pathways in age-related orthopedic diseases: focus on the fibroblast growth factor family.Military Medical Research · 2024Review
- Roles of Fibroblast Growth Factors in the Axon Guidance.International journal of molecular sciences · 2023Review
- FGF9 and FGF10 activate distinct signaling pathways to direct lung epithelial specification and branching.Science signaling · 2020Article
- Genetic insights into the mechanisms of Fgf signaling.Genes & development · 2016Review
- Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy.Cell metabolism · 2015Article
- Synthesis and mechanistic studies of a novel homoisoflavanone inhibitor of endothelial cell growth.PloS one · 2014Article
- Functional roles of fibroblast growth factor receptors (FGFRs) signaling in human cancers.Apoptosis : an international journal on programmed cell death · 2013Review
- Phosphorylation of serine 779 in fibroblast growth factor receptor 1 and 2 by protein kinase C(epsilon) regulates Ras/mitogen-activated protein kinase signaling and neuronal differentiation.The Journal of biological chemistry · 2013Article
- Changes in fibroblast growth factor-2 and FGF receptors in the frog visual system during optic nerve regeneration.Journal of chemical neuroanatomy · 2012Article
- Fibroblast growth factors in schizophrenia.Schizophrenia bulletin · 2010Review
- Molecular pathology of the fibroblast growth factor family.Human mutation · 2009Review
- Resident hepatocyte fibroblast growth factor receptor 4 limits hepatocarcinogenesis.Molecular carcinogenesis · 2009Article
- FGFR4 and its novel splice form in myogenic cells: Interplay of glycosylation and tyrosine phosphorylation.Journal of cellular physiology · 2008Article
- FGF signaling in the developing endochondral skeleton.Cytokine & growth factor reviews · 2005Review
- Role of SHP-2 in fibroblast growth factor receptor-mediated suppression of myogenesis in C2C12 myoblasts.Molecular and cellular biology · 2002Article
- Cell- and receptor isotype-specific phosphorylation of SNT1 by fibroblast growth factor receptor tyrosine kinases.In vitro cellular & developmental biology. Animal · 2002Article
- NF-kappa B signaling promotes both cell survival and neurite process formation in nerve growth factor-stimulated PC12 cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Stably transfected PC12 cell lines expressing similar amounts of chimeric receptors composed of the extracellular domain of the human platelet-derived growth factor (PDGF)beta receptor and the transmembrane and intracellular domains of the fibroblast growth factor receptors (FGFRs) 1, 3, and 4 undergo ligand-induced differentiation. The FGFR1 chimera (PFR1) is the most potent of the three, and PFR4 requires more frequent (every 24 hr) addition of ligand to maintain the response. Both PFR1 and -3 also show significant ligand-independent autophosphorylation but PFR4 does not. All of the chimeras activated phospholipase Cgamma, Shc, FGFR substrate (FRS)2, and the mitogen-activated protein kinases, ERK1 and 2. PFR4 was moderately weaker in stimulating these effects as well; PFR1 and -3 were comparable. None of the chimeras induced Sos association or were coprecipitated with Shc. Cotransfection of a dominant-negative Shc derivative, with tyrosine at 239, 240, and 317 replaced with phenylalanine, in the PFR-expressing cells was without effect on PDGF-induced neurite outgrowth. The same derivative substantially inhibited the response of these cells to NGF. These results indicate that FGFR1, 3, and 4 (i) are capable of signaling in a similar fashion; (ii) primarily use FRS2 and, perhaps, PLCgamma; and (iii) do not utilize Shc. The results also suggest that the principal difference between FGFR1, 3, and 4 is in the strength of the tyrosine kinase activity and that qualitative differences in signaling capacity are likely to be less important.
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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.