Muscarinic receptor-stimulated phosphoinositide turnover in human SK-N-SH neuroblastoma cells: differential inhibition by agents that elevate cyclic AMP.
Muscarinic receptor-stimulated phosphoinositide turnover in human SK-N-SH neuroblastoma cells: differential inhibition by agents that elevate cyclic AMP.
复制标题
人 SK-N-SH 神经母细胞瘤细胞中毒蕈碱受体刺激的磷酸肌醇更新：提高环 AMP 的药物的差异抑制。
DOI：
10.1111/j.1471-4159.1989.tb08541.x
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发表时间：
1989
影响因子：
4.7
通讯作者：
Fisher,SK
中科院分区：
文献类型：
--
作者：
Akil,M;Fisher,SK
The possibility that an increased intracellular concentration of cyclic AMP (cAMP) can regulate the extent of muscarinic receptor‐stimulated phosphoinositide (PPI) turnover in the human neuroblastoma cell line SK‐N‐SH was examined. Addition of either forskolin (or its water‐soluble nalog, L‐85,8051), theophylline, isobutylmethylxanthine, or Liolera toxin, agents that interact with either the catalytic unit of adenylate cyclase, cAMP phosphodiesterase, or the guanine nucleotide binding protein linked to adenylate cyclase activation, resulted in a 45–181% increase in cAMP concentration and a 27–70% inhibition of carbachol‐stimu‐lated inositol phosphate release. Through the use of digitonin‐permeabilized cells, the site of inhibition was localized to a step at, or distal to, the guanine nucleotide binding protein that regulates phospholipase C activity. In contrast, when intact SK‐N‐SH cells were exposed to prostaglandin E1, the ensuing increases in cAMP were not accompanied by an inhibition of stimulated PPI turnover. These differential effects of increased cAMP concentrations on stimulated PPI turnover may reflect the compartmentation of cAMP within SK‐N‐SH cells.
