Specific uncoupling by islet-activating protein, pertussis toxin, of negative signal transduction via alpha-adrenergic, cholinergic, and opiate receptors in neuroblastoma x glioma hybrid cells.

摘要: Exposure of NG108-15 hybrid cells to islet-activating protein (IAP), pertussis toxin, caused strong ADP-ribosylation one the membrane proteins with a molecular weight 41,000. This was paralleled by decreases in inhibition cAMP accumulation intact or associated reversal GTP-dependent adenylate cyclase, via alpha-adrenergic, cholinergic muscarinic, opiate receptors. The affinity these receptors for agonists lowered guanyl-5'-yl beta-gamma-imidodiphosphate (Gpp(NH)p) reflecting their coupling guanine nucleotide regulatory this cell line. effect Gpp(NH)p lost membranes IAP-treated cells; absence Gpp(NH)p, agonist lower treated than nontreated cells. In contrast, function bind antagonists remained unaltered Thus, IAP treatment specific uncoupling negative signal transduction from inhibitory cyclase catalytic unit protein, as result subunits protein.