ArticleMolecular and cellular biology1997
Enhanced signaling and morphological transformation by a membrane-localized derivative of the fibroblast growth factor receptor 3 kinase domain.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 68 citations in OpenAlex.
- Dual targeting of FGFR3 and ERBB3 enhances the efficacy of FGFR inhibitors in FGFR3 fusion-driven bladder cancer.BMC cancer · 2022Article
- Oncogenic fusion protein FGFR2-PPHLN1: Requirements for biological activation, and efficacy of inhibitors.Translational oncology · 2020Article
- Membrane-Associated, Not Cytoplasmic or Nuclear, FGFR1 Induces Neuronal Differentiation.Cells · 2019Article
- Oncogenic driver FGFR3-TACC3 is dependent on membrane trafficking and ERK signaling.Oncotarget · 2018Article
- SLC14A1: a novel target for human urothelial cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017Review
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- Differential regulation of FGFR3 by PTPN1 and PTPN2.Proteomics · 2015Article
- Structural mimicry of a-loop tyrosine phosphorylation by a pathogenic FGF receptor 3 mutation.Structure (London, England : 1993) · 2013Article
- PLZF regulates fibroblast growth factor responsiveness and maintenance of neural progenitors.PLoS biology · 2013Article
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- Nordihydroguaiaretic acid inhibits an activated fibroblast growth factor receptor 3 mutant and blocks downstream signaling in multiple myeloma cells.Cancer research · 2008Article
- FGF signaling inhibits the proliferation of human myeloma cells and reduces c-myc expression.BMC cell biology · 2003Article
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- Identification of tyrosine residues in constitutively activated fibroblast growth factor receptor 3 involved in mitogenesis, Stat activation, and phosphatidylinositol 3-kinase activation.Molecular biology of the cell · 2001Article
- Loss of heterozygosity at 4p16.3 and mutation of FGFR3 in transitional cell carcinoma.Oncogene · 2001Article
- Latent membrane protein 1 of Epstein-Barr virus inhibits as well as stimulates gene expression.Journal of virology · 2000Article
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- Import(ance) of growth factors in(to) the nucleus.The Journal of cell biology · 1999Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fibroblast growth factor (FGF) receptors (FGFRs) are membrane-spanning tyrosine kinase receptors that mediate regulatory signals for cell proliferation and differentiation in response to FGFs. We have previously determined that the Lys650-->Glu mutation in the activation loop of the kinase domain of FGFR3, which is responsible for the lethal skeletal dysplasia thanatophoric dyplasia type II (TDII), greatly enhances the ligand-independent kinase activity of the receptor. Here, we demonstrate that expression of this construct induces a c-fos promoter construct approximately 10-fold but does not lead to proliferation or morphological transformation of NIH 3T3 cells. In contrast, the isolated kinase domain of activated FGFR3, targeted to the plasma membrane by a myristylation signal, is able to stimulate c-fos expression by 40-fold, induce proliferation of quiescent cells, and morphologically transform fibroblasts. This result suggests that the extracellular and transmembrane domains of FGFRs exert a negative regulatory influence on the activity of the kinase domain. Targeting of the activated kinase domain to either the cytoplasm or the nucleus does not significantly affect biological signaling, suggesting that signals from FGFR3 resulting in mitogenesis originate exclusively from the plasma membrane. Furthermore, our novel observation that expression of a highly activated FGFR3 kinase domain is able to morphologically transform fibroblasts suggests that dysregulation of FGFR3 has the potential to play a role in human neoplasia.
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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.