scholarly journals Cell cycle regulation of astrocytes by extracellular nucleotides and fibroblast growth factor-2

2005 ◽  
Vol 1 (4) ◽  
pp. 329-336 ◽  
Author(s):  
Joseph T. Neary ◽  
Yuan Kang ◽  
You-Fang Shi
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cell Cycle Regulation ◽  
Extracellular Nucleotides ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Cycle Regulation

scholarly journals Exogenously Added Fibroblast Growth Factor 2 (FGF-2) to NIH3T3 CellsInteracts with Nuclear Ribosomal S6 Kinase 2 (RSK2) in a Cell Cycle-dependentManner*

2005 ◽  
Vol 280 (27) ◽  
pp. 25604-25610 ◽  
Author(s):  
Fabienne Soulet ◽  
Karine Bailly ◽  
Stéphane Roga ◽  
Anne-Claire Lavigne ◽  
François Amalric ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
S6 Kinase ◽  
Ribosomal S6 Kinase 2 ◽  
A Cell ◽  
Ribosomal S6 Kinase

scholarly journals The p107/E2F Pathway Regulates Fibroblast Growth Factor 2 Responsiveness in Neural Precursor Cells

2009 ◽  
Vol 29 (17) ◽  
pp. 4701-4713 ◽  
Author(s):  
Kelly A. McClellan ◽  
Jacqueline L. Vanderluit ◽  
Lisa M. Julian ◽  
Matthew G. Andrusiak ◽  
Delphie Dugal-Tessier ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factors ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Neural Progenitor ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Fibroblast Growth Factor 2 ◽  
Neural Precursor ◽  
Fibroblast Growth

ABSTRACT We have previously shown that p107, a member of the retinoblastoma (Rb) cell cycle regulatory family, has a unique function in regulating the pool of neural precursor cells. As the pool of progenitors is regulated by a limiting supply of trophic factors, we asked if the Rb/E2F pathway may control the size of the progenitor population by regulating the levels of growth factors or their receptors. Here, we demonstrate that fibroblast growth factor 2 (FGF2) is aberrantly upregulated in the brains of animals lacking Rb family proteins and that the gene encoding the FGF2 ligand is directly regulated by p107 and E2F3. Chromatin immunoprecipitation assays demonstrated that E2F3 and p107 occupy E2F consensus sites on the FGF2 promoter in the context of native chromatin. To evaluate the physiological consequence of FGF2 deregulation in both p107 and E2F3 mutants, we measured neural progenitor responsiveness to growth factors. Our results demonstrate that E2F3 and p107 are each mediators of FGF2 growth factor responsiveness in neural progenitor cells. These results support a model whereby p107 regulates the pool of FGF-responsive progenitors by directly regulating FGF2 gene expression in vivo. By identifying novel roles for p107/E2F in regulating genes outside of the classical cell cycle machinery targets, we uncover a new mechanism whereby Rb/E2F mediates proliferation through regulating growth factor responsiveness.

scholarly journals c-Myc protein is stabilized by fibroblast growth factor 2 and destabilized by ACTH to control cell cycle in mouse Y1 adrenocortical cells

2004 ◽  
Vol 33 (3) ◽  
pp. 623-638 ◽  
Author(s):  
Ana Paula Lepique ◽  
Miriam S Moraes ◽  
Kátia M Rocha ◽  
Claudia B Eichler ◽  
Glaucia N M Hajj ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Protein Kinase ◽  
Fibroblast Growth Factor ◽  
S Phase ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Adrenocortical Cells ◽  
Basal Expression ◽  
Phase Entry

ACTH is the hormone known to control adrenal cortex function and maintenance in the intact animal but, in culture, it inhibits proliferation of adrenocortical cells from different mammalian species, a puzzle that has remained unsolved for nearly 30 years. In this paper we compare ACTH and fibroblast growth factor 2 (FGF2) antagonistic effects on the cell cycle in the Y1 cell line, a functional lineage of mouse adreno-cortical tumor cells. This cell line displays chronic high levels of c-Ki-Ras-GTP, high active constitutive levels of phosphatidylinositol 3-OH kinase/Protein Kinase B (PI3K/AKT) and low constitutive basal expression of c-Myc, which accounts for a minor deregulation of the cell cycle. In G0/G1-arrested Y1 cells, over-expression of the dominant negative mutant HaRasN17 drastically reduces c-Ki-Ras-GTP levels, eliminating basal c-Myc expression and basal S phase entry. PI3K/Akt seems to be the downstream pathway from c-Ki-ras for deregulation of c-Myc basal expression, since wortmannin abolishes c-Myc expression in serum-starved, G0/G1-arrested Y1 cells. FGF2 is a strong mitogen for Y1 cells, promoting – in a manner dependent on the MEK/ERK pathway – c-myc transcription induction, c-Myc protein stabilization and S phase entry in G0/G1-arrested Y1 cells. On the other hand, ACTH causes c-Myc protein destabilization, partially blocking S phase entry induced by FGF2, by a process dependent on the cAMP/protein kinase A (PKA) pathway. The whole pathway activated by ACTH to destabilize c-Myc protein in Y1 cells might comprise the following steps: ACTH receptor →cAMP/PKA → Akt deactivation →GSK3 activity liberation → c-Myc Thr58 phosphorylation. We demonstrate that c-Myc regulation is a central key in the cell cycle control by these factors, since enforced expression of c-Myc through the MycER chimera abrogates the ACTH inhibitory effect over FGF2-induced S phase entry.

scholarly journals Fibroblast Growth Factor 2 Causes G2/M Cell Cycle Arrest in Ras-Driven Tumor Cells through a Src-Dependent Pathway

PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e72582 ◽  
Author(s):  
Jacqueline Salotti ◽  
Matheus H. Dias ◽  
Marianna M. Koga ◽  
Hugo A. Armelin
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Cell Cycle Arrest ◽  
Fibroblast Growth Factor ◽  
Tumor Cells ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
M Cell ◽  
Cycle Arrest ◽  
Dependent Pathway
Sign in / Sign up

Export Citation Format

Share Document