v-CRK, AN EFFECTOR OF THE NERVE GROWTH FACTOR SIGNALING PATHWAY, DELAYS APOPTOTIC CELL DEATH IN NEUROTROPHIN-DEPRIVED PC12 CELLS

1996 ◽  
Vol 24 (4) ◽  
pp. 573S-573S
Author(s):  
Robert H. Glassman ◽  
Barbara L. Hempstead ◽  
Hidesaburo Hanafusa ◽  
Raymond B. Birge
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Growth Factor Signaling ◽  
Nerve Growth ◽  
Growth Factor Signaling Pathway

scholarly journals v-Crk, an effector of the nerve growth factor signaling pathway, delays apoptotic cell death in neurotrophin-deprived PC12 cells

1996 ◽  
Vol 4 (1) ◽  
pp. 82-93 ◽  
Author(s):  
Robert H Glassman ◽  
Barbara L Hempstead ◽  
Lisa Staiano-Coico ◽  
Melissa G Steiner ◽  
Hidesaburo Hanafusa ◽  
...  
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Growth Factor Signaling ◽  
Nerve Growth ◽  
Growth Factor Signaling Pathway

scholarly journals Peroxisome Proliferator-activated Receptor γ Is a Novel Target of the Nerve Growth Factor Signaling Pathway in PC12 Cells

2005 ◽  
Vol 280 (10) ◽  
pp. 9604-9609 ◽  
Author(s):  
Karen M. Fuenzalida ◽  
Mauricio C. Aguilera ◽  
Daniela G. Piderit ◽  
Patricio C. Ramos ◽  
David Contador ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Peroxisome Proliferator ◽  
Growth Factor Signaling ◽  
Peroxisome Proliferator Activated Receptor ◽  
Nerve Growth ◽  
Novel Target ◽  
Growth Factor Signaling Pathway

Nerve growth factor prevents apoptotic cell death in injured central cholinergic neurons

1995 ◽  
Vol 359 (4) ◽  
pp. 573-585 ◽  
Author(s):  
Barbara J. Wilcox ◽  
Michael D. Applegate ◽  
Carlos Portera-Cailliau ◽  
Vassilis E. Koliatsos
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Apoptotic Cell ◽  
Cholinergic Neurons ◽  
Apoptotic Cell Death ◽  
Nerve Growth

scholarly journals Nerve growth factor withdrawal-induced cell death in neuronal PC12 cells resembles that in sympathetic neurons.

1992 ◽  
Vol 119 (6) ◽  
pp. 1669-1680 ◽  
Author(s):  
P W Mesner ◽  
T R Winters ◽  
S H Green
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Programmed Cell Death ◽  
Pc12 Cells ◽  
Sympathetic Neurons ◽  
Nerve Growth ◽  
Neuronal Pc12 Cells ◽  
New Protein

Previous studies have shown that in neuronal cells the developmental phenomenon of programmed cell death is an active process, requiring synthesis of both RNA and protein. This presumably reflects a requirement for novel gene products to effect cell death. It is shown here that the death of nerve growth factor-deprived neuronal PC12 cells occurs at the same rate as that of rat sympathetic neurons and, like rat sympathetic neurons, involves new transcription and translation. In nerve growth factor-deprived neuronal PC12 cells, a decline in metabolic activity, assessed by uptake of [3H]2-deoxyglucose, precedes the decline in cell number, assessed by counts of trypan blue-excluding cells. Both declines are prevented by actinomycin D and anisomycin. In contrast, the death of nonneuronal (chromaffin-like) PC12 cells is not inhibited by transcription or translation inhibitors and thus does not require new protein synthesis. DNA fragmentation by internucleosomal cleavage does not appear to be a consistent or significant aspect of cell death in sympathetic neurons, neuronal PC12 cells, or nonneuronal PC12 cells, notwithstanding that the putative nuclease inhibitor aurintricarboxylic acid protects sympathetic neurons, as well as neuronal and nonneuronal PC12 cells, from death induced by trophic factor removal. Both phenotypic classes of PC12 cells respond to aurintricarboxylic acid with similar dose-response characteristics. Our results indicate that programmed cell death in neuronal PC12 cells, but not in nonneuronal PC12 cells, resembles programmed cell death in sympathetic neurons in significant mechanistic aspects: time course, role of new protein synthesis, and lack of a significant degree of DNA fragmentation.

Protective effect of S-allyl-l-cysteine, a garlic compound, on amyloid β-protein-induced cell death in nerve growth factor-differentiated PC12 cells

2003 ◽  
Vol 46 (1) ◽  
pp. 119-125 ◽  
Author(s):  
Yoshihisa Ito ◽  
Yasuhiro Kosuge ◽  
Taeko Sakikubo ◽  
Kayo Horie ◽  
Natsue Ishikawa ◽  
...  
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Protective Effect ◽  
Pc12 Cells ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Nerve Growth ◽  
Differentiated Pc12 Cells ◽  
Β Protein
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