scholarly journals Testing the in vivo role of protein kinase C and c-fos in neurite outgrowth by microinjection of antibodies into PC12 cells.

1992 ◽  
Vol 3 (3) ◽  
pp. 323-333 ◽  
Author(s):  
J G Altin ◽  
R Wetts ◽  
K T Riabowol ◽  
R A Bradshaw
Keyword(s):  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Cellular Proliferation ◽  
Kinase C ◽  
Fos Protein ◽  
Induced Signal

To define the molecular bases of growth factor-induced signal transduction pathways, antibodies known to block the activity of either protein kinase C (PKC) or the fos protein were introduced into PC12 cells by microinjection. The antibody against PKC significantly inhibited neurite outgrowth when scored 24 h after microinjection and exposure to nerve growth factor (NGF). Microinjection of antibodies to fos significantly increased the percentage of neurite-bearing cells after exposure to either NGF or basic fibroblast growth factor (bFGF) but inhibited the stimulation of DNA synthesis by serum, suggesting that in PC12 cells, fos is involved in cellular proliferation. Thus, activation of PKC is involved in the induction of neurite outgrowth by NGF, but expression of the fos protein, which is induced by both NGF and bFGF, is not necessary and inhibits neurite outgrowth.

scholarly journals Nerve growth factor and fibroblast growth factor regulate neurite outgrowth and gene expression in PC12 cells via both protein kinase C- and cAMP-independent mechanisms.

1990 ◽  
Vol 110 (4) ◽  
pp. 1333-1339 ◽  
Author(s):  
D H Damon ◽  
P A D'Amore ◽  
J A Wagner
Keyword(s):  
Protein Kinase C ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Protein Kinase ◽  
Neurite Outgrowth ◽  
Fibroblast Growth Factor ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Fibroblast Growth ◽  
Kinase C

Nerve growth factor (NGF), acidic fibroblast growth factor (aFGF), and basic fibroblast growth factor (bFGF) promote the survival and differentiation of a variety of peripheral and central neurons. The signal transduction mechanisms that mediate the actions of these factors in neuronal cells are not well understood. We examined the effect of a deficiency in protein kinase C (PKC) and/or cAMP second messenger systems on the actions of NGF, aFGF, and bFGF in the pheochromocytoma (PC12) cell line. Activation of PKC was not required for NGF, aFGF, and bFGF to maximally induce ornithine decarboxylase (ODC), transcription of the early response genes, d2 and d5, or neurite outgrowth. In a PC12 cell mutant that is deficient in cAMP responsiveness (A126-1B2), all three growth factors maximally induced the transcription of d5 and neurite outgrowth, but aFGF and bFGF did not induce significant increases in ODC. NGF and aFGF maximally induced the transcription of d2 in A126-1B2 cells, but bFGF-induced d2 transcription was attenuated. NGF, aFGF, and bFGF maximally induced neurite outgrowth and d5 transcription in A126 cells that were made deficient in PKC. The d2 transcriptional response was substantially reduced in cells deficient in both PKC and cAMP responsiveness. These observations lead us to conclude that (a) cAMP- and PKC-dependent events are, at least in part, causally linked to NGF, aFGF, and bFGF induction of both ODC and transcription of d2 and may control functionally redundant pathways; (b) NGF, aFGF, and bFGF can elicit neurite outgrowth and increase transcription of d2 and d5 in PC12 cells via mechanisms that are independent of both PKC and cAMP; (c) NGF, aFGF, and bFGF can induce ODC in the absence of PKC; and (d) aFGF and bFGF require cAMP responsiveness to induce ODC in PC12 cells.

scholarly journals Nuclear diacylglycerol is increased during cell proliferation in vivo

1993 ◽  
Vol 290 (3) ◽  
pp. 633-636 ◽  
Author(s):  
H Banfić ◽  
M Žižak ◽  
N Divecha ◽  
R F Irvine
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Nuclear Membrane ◽  
Cellular Proliferation ◽  
Detectable Change ◽  
Renal Growth ◽  
Kinase C ◽  
Stimulation Of

Highly purified nuclei were prepared from livers and kidneys of rats undergoing compensatory hepatic or renal growth, the former being predominantly by cellular proliferation, and the latter mostly by cellular enlargement. In liver, an increase in nuclear diacylglycerol (DAG) concentration occurred between 16 and 30 h, peaking at around 20 h. At the peak of nuclear DAG production a specific translocation of protein kinase C to the nucleus could be detected; no such changes occurred in kidney. There was no detectable change in whole-cell DAG levels in liver, and the increase in DAG was only measurable in nuclei freed of their nuclear membrane. Overall, these results suggest that there is a stimulation of intranuclear DAG production, possibly through the activation of an inositide cycle [Divecha, Banfić and Irvine (1991) EMBO J. 10, 3207-3214] during cell proliferation in vivo.

Nerve growth factor enhances the level of the protein kinase C substrate B-50 in pheochromocytoma PC12 cells

1986 ◽  
Vol 139 (2) ◽  
pp. 644-651 ◽  
Author(s):  
C.O.M. Van Hooff ◽  
P.N.E. De Graan ◽  
J. Boonstra ◽  
A.B. Oestreicher ◽  
M.H. Schmidt-Michels ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Protein Kinase ◽  
Pc12 Cells ◽  
Nerve Growth ◽  
Kinase C ◽  
Pheochromocytoma Pc12 ◽  
Pheochromocytoma Pc12 Cells
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