Role of PP2A in Chondrocyte Cell Cycle Arrest by FGF
Author Information
Author(s): Victoria Kolupaeva, Emmanuel Laplantine, Claudio Basilico
Primary Institution: New York University School of Medicine
Hypothesis
Does p107 dephosphorylation play a critical role in the chondrocyte response to FGF?
Conclusion
p107 dephosphorylation is a key event in FGF-induced cell cycle arrest in chondrocytes, mediated by the PP2A phosphatase.
Supporting Evidence
- FGF signaling inhibits chondrocyte proliferation.
- p107 dephosphorylation is one of the earliest events in FGF-induced growth arrest.
- Overexpression of cyclin D1/cdk4 prevents p107 dephosphorylation and growth arrest.
- PP2A is activated by FGF to promote p107 dephosphorylation.
- Inhibition of PP2A prevents FGF-induced p107 dephosphorylation.
- Knockdown of PP2A delays p107 dephosphorylation and allows continued cell cycle progression.
Takeaway
When chondrocytes are treated with FGF, a protein called p107 gets changed in a way that stops the cells from growing. This change is helped by another protein called PP2A.
Methodology
The study involved overexpressing cyclin D1/cdk4 in RCS chondrocytes and analyzing the effects on p107 dephosphorylation and cell cycle arrest.
Limitations
The study did not isolate pure populations of cells with reduced levels of PP2A due to lethality of PP2A knockdown.
Digital Object Identifier (DOI)
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