ArticleThe Journal of cell biology2002
FGF signaling targets the pRb-related p107 and p130 proteins to induce chondrocyte growth arrest.
Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 57 citations in OpenAlex.
- FGF19 induces the cell cycle arrest at G2-phase in chondrocytes.Cell death discovery · 2023Article
- MPSI Manifestations and Treatment Outcome: Skeletal Focus.International journal of molecular sciences · 2022Review
- Phosphoproteomics of Fibroblast Growth Factor 1 (FGF1) Signaling in Chondrocytes: Identifying the Signature of Inhibitory Response.Molecular & cellular proteomics : MCP · 2017Article
- Achondroplasia: Development, pathogenesis, and therapy.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Review
- Cell type-specific control of protein synthesis and proliferation by FGF-dependent signaling to the translation repressor 4E-BP.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- FGF signaling in the osteoprogenitor lineage non-autonomously regulates postnatal chondrocyte proliferation and skeletal growth.Development (Cambridge, England) · 2016Article
- The Indispensable Role of Cyclin-Dependent Kinase 1 in Skeletal Development.Scientific reports · 2016Article
- Fibroblast growth factor signaling in skeletal development and disease.Genes & development · 2015Review
- PP2A: more than a reset switch to activate pRB proteins during the cell cycle and in response to signaling cues.Cell cycle (Georgetown, Tex.) · 2015Review
- Altered signaling in the G1 phase deregulates chondrocyte growth in a mouse model with proteoglycan undersulfation.Journal of cellular biochemistry · 2014Article
- Differential gene expression of the intermediate and outer interzone layers of developing articular cartilage in murine embryos.Stem cells and development · 2014Article
- Loss of the mammalian DREAM complex deregulates chondrocyte proliferation.Molecular and cellular biology · 2014Article
- The B55α regulatory subunit of protein phosphatase 2A mediates fibroblast growth factor-induced p107 dephosphorylation and growth arrest in chondrocytes.Molecular and cellular biology · 2013Article
- Activation of p107 by fibroblast growth factor, which is essential for chondrocyte cell cycle exit, is mediated by the protein phosphatase 2A/B55α holoenzyme.Molecular and cellular biology · 2013Article
- Genetic determinants of phosphate response in Drosophila.PloS one · 2013Article
- Overexpression of cyclin E/CDK2 complexes overcomes FGF-induced cell cycle arrest in the presence of hypophosphorylated Rb proteins.Cell cycle (Georgetown, Tex.) · 2012Article
- Review
- FGF inhibits the activity of the cyclin B1/CDK1 kinase to induce a transient G₂arrest in RCS chondrocytes.Cell cycle (Georgetown, Tex.) · 2010Article
- Article
- Disruption of calvarial ossification in E2f4 mutant embryos correlates with increased proliferation and progenitor cell populations.Cell cycle (Georgetown, Tex.) · 2010Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Unregulated FGF signaling affects endochondral ossification and long bone growth, causing several genetic forms of human dwarfism. One major mechanism by which FGFs regulate endochondral bone growth is through their inhibitory effect on chondrocyte proliferation. Because mice with targeted mutations of the retinoblastoma (Rb)-related proteins p107 and p130 present severe endochondral bone defects with excessive chondrocyte proliferation, we have investigated the role of the Rb family of cell cycle regulators in the FGF response. Using a chondrocyte cell line, we found that FGF induced a rapid dephosphorylation of all three proteins of the Rb family (pRb, p107, and p130) and a blockade of the cells in the G1 phase of the cell cycle. This cell cycle block was reversed by inactivation of Rb proteins with viral oncoproteins such as polyoma large T (PyLT) antigen and Adenovirus E1A. Expression of a PyLT mutant that efficiently binds pRb, but not p107 and p130, allowed the cells to be growth inhibited by FGF, suggesting that pRb itself is not involved in the FGF response. To investigate more precisely the role of the individual Rb family proteins in FGF-mediated growth inhibition, we used chondrocyte micromass culture of limb bud cells isolated from mice lacking Rb proteins individually or in combination. Although wild-type as well as Rb-/- chondrocytes were similarly growth inhibited by FGF, chondrocytes null for p107 and p130 did not respond to FGF. Furthermore, FGF treatment of metatarsal bone rudiments obtained from p107-/-;p130-/- embryos failed to inhibit proliferation of growth plate chondrocytes, whereas rudiments from p107-null or p130-null embryos showed only a slight inhibition of growth. Our findings indicate that p107 and p130, but not pRb, are critical effectors of FGF-mediated growth inhibition in chondrocytes.
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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.