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毒蕈碱受体介导的SK-N-SH人神经母细胞瘤细胞中环磷酸腺苷(cAMP)水平升高。

Muscarinic receptor-mediated increase in cAMP levels in SK-N-SH human neuroblastoma cells.

作者信息

Baumgold J, Fishman P H

机构信息

Membrane Biochemistry Section, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, MD 20892.

出版信息

Biochem Biophys Res Commun. 1988 Aug 15;154(3):1137-43. doi: 10.1016/0006-291x(88)90259-8.

Abstract

Stimulation of muscarinic cholinergic receptors in SK-N-SH human neuroblastoma cells resulted in a 1.5-4 fold increase in intracellular cAMP levels. This unusual response was sensitive to atropine and pirenzepine but insensitive to pertussis toxin. It was observable regardless of whether basal, PGE1- or forskolin-stimulated cAMP levels were measured. The half-maximal concentration for carbachol-stimulation of cAMP levels (6 microM) was similar to that for the previously determined carbachol-induced stimulation of phosphoinositide turnover in these cells, suggesting that the former is mediated by the latter. These data indicate that cross-talk between the phosphoinositide turnover system and the adenylate cyclase system results in increased cAMP levels in SK-N-SH cells in response to muscarinic receptor stimulation.

摘要

刺激SK-N-SH人神经母细胞瘤细胞中的毒蕈碱胆碱能受体,导致细胞内cAMP水平增加了1.5至4倍。这种异常反应对阿托品和哌仑西平敏感,但对百日咳毒素不敏感。无论测量基础的、PGE1或福斯高林刺激的cAMP水平,均可观察到这种反应。卡巴胆碱刺激cAMP水平的半数最大浓度(6 microM)与先前测定的这些细胞中卡巴胆碱诱导的磷酸肌醇代谢周转刺激的浓度相似,这表明前者是由后者介导的。这些数据表明,磷酸肌醇代谢周转系统和腺苷酸环化酶系统之间的相互作用导致SK-N-SH细胞中cAMP水平因毒蕈碱受体刺激而增加。

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