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Platelet-activating factor activates a Ca(2+)-dependent K+ channel which is not involved in c-fos expression in human
W Di Berardino1, I Bourget, H Schmid-Antomarchi
1Laboratoire d'Immunologie Cellulaire et Moléculaire INSERM U364, Faculté de Médecine (Pasteur), Nice, France.
Abstract:
In this report, it is shown that the platelet-activating factor (PAF) induced, in human B lymphoblastoid cells, 86Rb+ influx and efflux suggesting that it activated a K+ channel. Opening of this channel was dependent on PAF-induced Ca2+ mobilization. Ionomycin and thapsigargin--a specific inhibitor of (Ca(2+)-Mg2+)-ATPase--mimicked the effect of PAF both on intracellular calcium and activation of the channel. This channel was inhibited by charybdotoxin, high doses of tetraethylammonium and barium but was insensitive to apamin, 4-aminopyridine. These features indicate that PAF activated a Ca(2+)-dependent K+ channel. In these cells, PAF also induced the expression of c-fos oncogene. This effect was not affected by charybdotoxin indicating that this channel is not involved in the control of early gene transcription.