ArticleBone2010
FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence.
Article in Bone, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 59 citations in OpenAlex.
- Structure-function relationship in FGF signaling: rational design of highly stable FGF2 variants and their effect on cell growth, metabolism, and survival.Journal of biological engineering · 2026Article
- Advances in the mechanism and therapies of achondroplasia.Genes & diseases · 2025Review
- Specific inhibition of fibroblast growth factor receptor 1 signaling by a DNA aptamer.Molecular therapy. Nucleic acids · 2025Article
- Achondroplasia: aligning mouse model with human clinical studies shows crucial importance of immediate postnatal start of the therapy.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Quantitative and qualitative differences in the activation of a fibroblast growth factor receptor by different FGF ligands.Cytokine & growth factor reviews · 2024Review
- Article
- The role of fibroblast growth factor 8 in cartilage development and disease.Journal of cellular and molecular medicine · 2022Review
- FGF-2 induces a failure of cell cycle progression in cells harboring amplified K-Ras, revealing new insights into oncogene-induced senescence.Molecular omics · 2021Article
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- The inositol phosphatase SHIP2 enables sustained ERK activation downstream of FGF receptors by recruiting Src kinases.Science signaling · 2018Article
- C-type natriuretic peptide analog treatment of craniosynostosis in a Crouzon syndrome mouse model.PloS one · 2018Article
- Inhibitor repurposing reveals ALK, LTK, FGFR, RET and TRK kinases as the targets of AZD1480.Oncotarget · 2017Article
- An inactivating mutation in intestinal cell kinase, ICK, impairs hedgehog signalling and causes short rib-polydactyly syndrome.Human molecular genetics · 2016Article
- Effect of the achondroplasia mutation on FGFR3 dimerization and FGFR3 structural response to fgf1 and fgf2: A quantitative FRET study in osmotically derived plasma membrane vesicles.Biochimica et biophysica acta · 2016Article
- Regulation of Long Bone Growth in Vertebrates; It Is Time to Catch Up.Endocrine reviews · 2015Review
- Article
- Instability restricts signaling of multiple fibroblast growth factors.Cellular and molecular life sciences : CMLS · 2015Article
- FGFR3 Deficiency Causes Multiple Chondroma-like Lesions by Upregulating Hedgehog Signaling.PLoS genetics · 2015Article
- Wnt5A promotes an adaptive, senescent-like stress response, while continuing to drive invasion in melanoma cells.Pigment cell & melanoma research · 2015Article
- H-Ras-driven tumoral maintenance is sustained through caveolin-1-dependent alterations in calcium signaling.Oncogene · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Oncogenic activation of the RAS-ERK MAP kinase signaling pathway can lead to uncontrolled proliferation but can also result in apoptosis or premature cellular senescence, both regarded as natural protective barriers to cell immortalization and transformation. In FGFR3-related skeletal dyplasias, oncogenic mutations in the FGFR3 receptor tyrosine kinase cause profound inhibition of cartilage growth resulting in severe dwarfism, although many of the precise mechanisms of FGFR3 action remain unclear. Mutated FGFR3 induces constitutive activation of the ERK pathway in chondrocytes and, remarkably, can also cause both increased proliferation and apoptosis in growing cartilage, depending on the gestational age. Here, we demonstrate that FGFR3 signaling is also capable of inducing premature senescence in chondrocytes, manifested as reversible, ERK-dependent growth arrest accompanied by alteration of cellular shape, loss of the extracellular matrix, upregulation of senescence markers (alpha-GLUCOSIDASE, FIBRONECTIN, CAVEOLIN 1, LAMIN A, SM22alpha and TIMP 1), and induction of senescence-associated beta-GALACTOSIDASE activity. Our data support a model whereby FGFR3 signaling inhibits cartilage growth via exploiting cellular responses originally designed to eliminate cells harboring activated oncogenes.
Indexed as
Identifiers
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.