Basic fibroblast growth factor inhibits p38-mediated cell differentiation and growth inhibition by activin A but not by histone deacetylase inhibitors in CML cells

2007 ◽  
Vol 87 (3) ◽  
pp. 175-182 ◽  
Author(s):  
Chun-Hsin Chen ◽  
John Yi-Chung Lin ◽  
Fu-Hwa Liu ◽  
Ju-Ling Chang ◽  
Huei-Mei Huang
Keyword(s):  
Cell Differentiation ◽  
Growth Factor ◽  
Growth Inhibition ◽  
Fibroblast Growth Factor ◽  
Histone Deacetylase ◽  
Basic Fibroblast Growth Factor ◽  
Histone Deacetylase Inhibitors ◽  
Activin A ◽  
Fibroblast Growth

Induction of activin A is essential for the neuroprotective action of basic fibroblast growth factor in vivo

10.1038/77548 ◽  
2000 ◽  
Vol 6 (7) ◽  
pp. 812-815 ◽  
Author(s):  
Yvonne P. Tretter ◽  
Moritz Hertel ◽  
Barbara Munz ◽  
Gerrit ten Bruggencate ◽  
Sabine Werner ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Activin A ◽  
Fibroblast Growth ◽  
Neuroprotective Action

scholarly journals Synergistic activity of activin A and basic fibroblast growth factor on tyrosine hydroxylase expression through Smad3 and ERK1/ERK2 MAPK signaling pathways

2005 ◽  
Vol 184 (3) ◽  
pp. 493-504 ◽  
Author(s):  
Y L Bao ◽  
K Tsuchida ◽  
B Liu ◽  
A Kurisaki ◽  
T Matsuzaki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tyrosine Hydroxylase ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Nuclear Translocation ◽  
Specific Inhibitor ◽  
Mapk Signaling ◽  
Activin A ◽  
Synergistic Activity ◽  
Fibroblast Growth

Activin has previously been shown to act as a nerve cell survival factor and to have neurotrophic effects on neurons. However, the role of activin in regulating neurotransmitter expression in the central nervous system and the exact mechanisms involved in this process are poorly understood. In the present study, we report that activin A and basic fibroblast growth factor (bFGF) synergistically increased the protein level of tyrosine hydroxylase (TH), and also greatly increased the TH mRNA level, in both mouse E14 striatal primary cell cultures and the hippocampal neuronal cell line HT22. Activin A and bFGF cooperatively stimulated nuclear translocation of Smad3 and specifically activated ERK1/2, but not p38 or JNK. Interestingly, a specific inhibitor for MEK, U0126, efficiently blocked the induction of TH promoter activity by activin A and bFGF, indicating that activin A collaborated with bFGF signaling to induce the TH gene through selective activation of ERK-type MAP kinase in mouse striatal and HT22 cells. These data suggest that activin A may act in concert with bFGF for the development of TH-positive neurons.

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