Multiple agents rescue PC12 cells from serum-free cell death by translation- and transcription-independent mechanisms
TL;DR: Findings indicate that survival was promoted by mechanisms that do not require synthesis of RNA or protein, and Regulation of protein kinase activity appears to be a common feature of each pathway and may play a key convergent role in mediating prevention of cell death.
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Abstract: Past studies revealed that NGF and fibroblast growth factor (FGF) prevent the death of PC 12 pheochromocytoma cells that otherwise occurs in serum-free medium. Additional agents were tested here for their abilities to promote long-term survival of naive and NGF-pretreated (primed) PC 12 cells in serum-free conditions. Forskolin and permeant cAMP analogs effectively prevented serum-free cell death, as did micromolar levels of insulin and 10-100-nM levels of insulin-like growth factors I and II. In contrast to NGF and FGF, none of these agents caused neuronal differentiation of naive cells or neurite regeneration by primed cells. Each of the agents also prevented rapid cell death in a balanced salt solution, thus apparently ruling out a mechanism dependent on regulation of nutrient uptake. Epidermal growth factor and elevated K+ appeared to slow the rate of cell death, but did not promote long-term survival; phorbol ester, dexamethasone, or vanadate did not prevent cell death. Each of the survival-promoting agents was effective even when macromolecular synthesis was blocked. Because the synthesis inhibitors themselves did not significantly prevent cell death, such findings indicate that survival was promoted by mechanisms that do not require synthesis of RNA or protein. In addition, various lines of experimental evidence (using the kinase inhibitor K-252a or PC 12 cell variants deficient either in protein kinase A activity or in responsiveness to NGF) further suggested that the effective agents maintain survival by independent initial pathways. Regulation of protein kinase activity appears to be a common feature of each pathway and may therefore play a key convergent role in mediating prevention of cell death.
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Effect of protein synthesis inhibitors on growth factor activation of c-fos, c-myc, and actin gene transcription.
TL;DR: The results suggest that in PC12 cells c-fos transcription is activated by a protein-synthesis-independent mechanism, whereas c-myc stimulation requires new protein synthesis.
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Selective and nonselective stimulation of central cholinergic and dopaminergic development in vitro by nerve growth factor, basic fibroblast growth factor, epidermal growth factor, insulin and the insulin-like growth factors I and II
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TL;DR: The hypothesis that insulin and its homologs belong to a broad family of neuritogenic polypeptides is supported, as it is shown that insulin acts on the same, or a subpopulation, of NGF-responsive neurons.
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Sarcoma viruses carrying ras oncogenes induce differentiation-associated properties in a neuronal cell line
Makoto Noda,Minoru S.H. Ko,Akihiko Ogura,Ding Gan Liu,Takehiko Amano,Toshiya Takano,Yoji Ikawa +6 more
TL;DR: It is found that Ki- and Ha-MSV mimic some, if not all, of the activities of NGF in PC12 cells, and there is evidence that the viral oncogenes, v-Ki-ras and v-Ha-ras, are responsible for this phenomenon.
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