ArticlePloS one2008
PP2A-mediated dephosphorylation of p107 plays a critical role in chondrocyte cell cycle arrest by FGF.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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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
27 citing papers in PubMed, 38 citations in OpenAlex.
- Senescence-Associated Checkpoint Gene Dysregulation in Established Osteoarthritis: Integrated Transcriptomic Analysis and In Vitro Evaluation of CDK6 and WEE1.Biomedicines · 2026Article
- PP2Ac Regulates Autophagy via Mediating mTORC1 and ULK1 During Osteoclastogenesis in the Subchondral Bone of Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- FGF19 induces the cell cycle arrest at G2-phase in chondrocytes.Cell death discovery · 2023Article
- PP2A as the Main Node of Therapeutic Strategies and Resistance Reversal in Triple-Negative Breast Cancer.Molecules (Basel, Switzerland) · 2017Review
- 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
- Clinicopathological effects of protein phosphatase 2, regulatory subunit A, alpha mutations in gastrointestinal stromal tumors.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016Article
- 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
- Protein phosphatase 2A promotes the transition to G0 during terminal differentiation in Drosophila.Development (Cambridge, England) · 2015Article
- 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
- A Network Map of FGF-1/FGFR Signaling System.Journal of signal transduction · 2014Review
- 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
- Cyclin D1 overexpression perturbs DNA replication and induces replication-associated DNA double-strand breaks in acquired radioresistant cells.Cell cycle (Georgetown, Tex.) · 2013Article
- Article
- A new mode of cell cycle stimulation: cyclin E and CDK2-mediated cytoplasmic retention of repressive E2F complexes.Cell cycle (Georgetown, Tex.) · 2012Article
- 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
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
FGF signaling inhibits chondrocyte proliferation, a cell type-specific response that is the basis for several genetic skeletal disorders caused by activating FGFR mutations. This phenomenon requires the function of the p107 and p130 members of the Rb protein family, and p107 dephosphorylation is one of the earliest distinguishing events in FGF-induced growth arrest. To determine whether p107 dephoshorylation played a critical role in the chondrocyte response to FGF, we sought to counteract this process by overexpressing in RCS chondrocytes the cyclin D1/cdk4 kinase complex. CyclinD/cdk4-expressing RCS cells became resistant to FGF-induced p107 dephosphorylation and growth arrest, and maintained significantly high levels of cyclin E/cdk2 activity and of phosphorylated p130 at later times of FGF treatment. We explored the involvement of a phosphatase in p107 dephosphorylation. Expression of the SV40 small T-Ag, which inhibits the activity of the PP2A phosphatase, or knockdown of the expression of the PP2A catalytic subunit by RNA interference prevented p107 dephosphorylation and FGF-induced growth arrest of RCS cells. Furthermore, an association between p107 and PP2A was induced by FGF treatment. Our data show that p107 dephosphorylation is a key event in FGF-induced cell cycle arrest and indicate that in chondrocytes FGF activates the PP2A phosphatase to promote p107 dephosphorylation.
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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.