The levels of intracellular calcium [Ca 2+ ]i were examined in CO25 myoblast cells bearing a mutated human N-ras oncogene, after stimulation by thapsigargin (ThG), bombesin and epidermal growth factor (EGF). Thapsigargin induced a [Ca 2+ ]i rise mostly from intracellular calcium pools, and a small Ca 2+ entry into cytoplasm via the plasma membrane channel. In both ras-induced and differentiated CO25 cells, [Ca 2+ ]i increase showed a similar pattern of events after addition of ThG. The addition of EGF and bombesin to both ras-induced and differentiated cells did not induce Ca 2+ mobilization, suggesting that the cells may not have receptors for the ligands, or desensitization of the receptors may have occured by a different signalling pathway such as stimulation of protein kinase C activity.

The levels of intracellular calcium [Ca 2+ ]i were examined in CO25 myoblast cells bearing a mutated human N-ras oncogene, after stimulation by thapsigargin (ThG), bombesin and epidermal growth factor (EGF). Thapsigargin induced a [Ca 2+ ]i rise mostly from intracellular calcium pools, and a small Ca 2+ entry into cytoplasm via the plasma membrane channel. In both ras-induced and differentiated CO25 cells, [Ca 2+ ]i increase showed a similar pattern of events after addition of ThG. The addition of EGF and bombesin to both ras-induced and differentiated cells did not induce Ca 2+ mobilization, suggesting that the cells may not have receptors for the ligands, or desensitization of the receptors may have occured by a different signalling pathway such as stimulation of protein kinase C activity.