Calcium, cyclic AMP and protein kinase C--partners in mitogenesis.
Evidence is steadily mounting that the proto-oncogenes, whose products organize and start the programs that drive normal eukaryotic cells through their chromosome replication/mitosis cycles, are transiently stimulated by sequential signals from a multi-purpose, receptor-operated mechanism (consisting of internal surges of Ca2+ and bursts of protein kinase C activity resulting from phosphatidylinositol 4,5-bisphosphate breakdown and the opening of membrane Ca2+ channels induced by receptor-associated tyrosine-protein kinase activity) and bursts of cyclic AMP-dependent kinase activity. The bypassing or subversion of the receptor-operated Ca2+/phospholipid breakdown/protein kinase C signalling mechanism is probably the basis of the freeing of cell proliferation from external controls that characterizes all neoplastic transformations.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D002453:Cell Cycle; D000242:Cyclic AMP / Q000502:physiology*; D004261:DNA Replication; D006801:Humans; D008938:Mitosis; D011493:Protein Kinase C / Q000502:physiology*; D011519:Proto-Oncogenes
D000242:Cyclic AMP; D011493:Protein Kinase C; D002118:Calcium