scholarly journals Basic fibroblast growth factor-induced translocation of p21-activated kinase to the membrane is independent of phospholipase C-γ1 in the differentiation of PC12 cells

2002 ◽  
Vol 34 (2) ◽  
pp. 172-176 ◽  
Author(s):  
Kyung-Sun Shin ◽  
Eun-Young Shin ◽  
Chan-Soo Lee ◽  
Song-Hua Quan ◽  
Kyung-Nam Woo ◽  
...  
Keyword(s):  
Growth Factor ◽  
Phospholipase C ◽  
Fibroblast Growth Factor ◽  
Pc12 Cells ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
P21 Activated Kinase

Characterization of an endooligopeptidase A-like protein in PC12 cells: Activity modulation by cAMP but not by basic fibroblast growth factor

1995 ◽  
Vol 57 (2) ◽  
pp. 311-320 ◽  
Author(s):  
Emer S. Ferro ◽  
Denise V. Tambourgy ◽  
Patricia A. E. Abreu ◽  
Antonio C. M. Camargo ◽  
Isaias Raw ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Pc12 Cells ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth

scholarly journals Overexpression of phospholipase C-gamma in NIH 3T3 fibroblasts results in increased phosphatidylinositol hydrolysis in response to platelet-derived growth factor and basic fibroblast growth factor.

1990 ◽  
Vol 10 (11) ◽  
pp. 6069-6072 ◽  
Author(s):  
A Cuadrado ◽  
C J Molloy
Keyword(s):  
Growth Factor ◽  
Phospholipase C ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Platelet Derived Growth Factor ◽  
Phosphoinositide Metabolism ◽  
Fibroblast Growth ◽  
3T3 Fibroblasts ◽  
Phospholipase C Gamma ◽  
Nih 3T3

Overexpression of phospholipase C-gamma in fibroblasts led to increased tyrosine phosphorylation of this enzyme in response to platelet-derived growth factor and basic fibroblast growth factor. This correlated with increased phosphoinositide release but not with enhanced mitogenicity. Thus, phospholipase C-gamma-mediated phosphoinositide metabolism may not be limiting in the signaling pathways initiated by these growth factors.

Overexpression of phospholipase C-gamma in NIH 3T3 fibroblasts results in increased phosphatidylinositol hydrolysis in response to platelet-derived growth factor and basic fibroblast growth factor

1990 ◽  
Vol 10 (11) ◽  
pp. 6069-6072
Author(s):  
A Cuadrado ◽  
C J Molloy
Keyword(s):  
Growth Factor ◽  
Phospholipase C ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Platelet Derived Growth Factor ◽  
Phosphoinositide Metabolism ◽  
Fibroblast Growth ◽  
3T3 Fibroblasts ◽  
Phospholipase C Gamma ◽  
Nih 3T3

Overexpression of phospholipase C-gamma in fibroblasts led to increased tyrosine phosphorylation of this enzyme in response to platelet-derived growth factor and basic fibroblast growth factor. This correlated with increased phosphoinositide release but not with enhanced mitogenicity. Thus, phospholipase C-gamma-mediated phosphoinositide metabolism may not be limiting in the signaling pathways initiated by these growth factors.

Neurite outgrowth from PC12 cells by basic fibroblast growth factor (bFGF) is mediated by RhoA inactivation through p190RhoGAP and ARAP3

2010 ◽  
Vol 224 (3) ◽  
pp. 786-794 ◽  
Author(s):  
Chan-Young Jeon ◽  
Hee-Jun Kim ◽  
Hiroshi Morii ◽  
Nozomu Mori ◽  
Jeffrey Settleman ◽  
...  
Keyword(s):  
Growth Factor ◽  
Neurite Outgrowth ◽  
Fibroblast Growth Factor ◽  
Pc12 Cells ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth

scholarly journals Divergence in the anti-apoptotic signalling pathways used by nerve growth factor and basic fibroblast growth factor (bFGF) in PC12 cells: rescue by bFGF involves protein kinase Cδ

2000 ◽  
Vol 352 (1) ◽  
pp. 175-182 ◽  
Author(s):  
Maribeth M. WERT ◽  
H. Clive PALFREY
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Protein Kinase ◽  
Map Kinase ◽  
Fibroblast Growth Factor ◽  
Pc12 Cells ◽  
Basic Fibroblast Growth Factor ◽  
Dominant Negative ◽  
Signalling Pathways ◽  
Fibroblast Growth

The mechanisms whereby nerve growth factor (NGF) and basic fibroblast growth factor (bFGF) block apoptosis in serum-deprived PC12 cells were investigated. NGF, but not bFGF, strongly activated Akt/protein kinase B, a downstream effector of phosphoinositide (phosphatidylinositol) 3-kinase (PI 3-kinase). In addition, inhibition of PI 3-kinase by LY294002 partially blocked inhibition of apoptosis by NGF, but not that by bFGF, suggesting divergence in NGF and bFGF anti-apoptotic signalling pathways. Both growth factors strongly activated mitogen-activated protein (MAP) kinases, but blockade of signalling through this pathway, either by the expression of dominant-negative Ras or by treatment with the MAP kinase/ERK kinase (MEK) inhibitor U0126, partially inhibited only bFGF, but not NGF, anti-apoptotic signalling. Use of isoform-specific protein kinase C (PKC) inhibitors such as bisindoylmaleimide-I and Gö 6983 suggested that PKCδ is a likely component of bFGF trophic signalling. A role for PKCδ was confirmed in PC12 cells expressing a dominant-negative PKCδ fragment, in which reversal of apoptosis by bFGF was partially blocked. The PKCδ signal was not mediated by the MAP kinase cascade, as bFGF activation of this pathway was not affected in cells expressing the dominant-negative PKCδ fragment. Full inhibition of bFGF anti-apoptotic signalling occurred when both the PKCδ and Ras/MAP kinase pathways were inhibited. Together, these data demonstrate that inhibition of apoptosis by bFGF in PC12 cells operates differently from that mediated by NGF, requiring the addition of signals from both the Ras/MAP kinase and PKC signalling pathways.

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