Abstract

Depolarized stimulation 1.5-fold increased Ca 2+ influx which was inhibited by pretreatment with verapamil or LaCl 3. Treatment with pertussis toxin, islet-activating protein (IAP), induced a reduction in 50 mM K +- induced Ca 2+ influx and stimulated adenylate cyclase (AC) activity in NG108-15 cells. However, addition of dibutyryl cAMP or forskolin treatment elevating cAMP level exerted no effects on a depolarization-induced Ca 2+ influx. Dissociated B-oligomer of IAP after treatment with dithiothreitol and ATP increased a depolarization-evoked Ca 2+ influx. It is suggested that inhibitory GTP-binding protein (G i) or other IAP substrate proteins could directly be involved in Ca 2+ influx via voltage-sensitive Ca 2+ channel.

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