毒蕈碱胆碱能受体诱导的pge1刺激的神经母细胞瘤X胶质瘤细胞cAMP积累增强:百日咳毒素预防。

J M Thomas, B B Hoffman
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引用次数: 0

摘要

用毒蕈碱胆碱能激动剂carbachol慢性治疗神经母细胞瘤X胶质瘤杂交细胞(NG 108-15),可急性抑制腺苷酸环化酶,导致pge1刺激的cAMP积累增加104 +/- 10%。百日咳毒素预处理完整细胞可通过adp -核糖基化对抑制调节蛋白Gi进行结构修饰,从而消除氨基酚的急性抑制作用。百日咳毒素预处理细胞也导致pge1刺激的cAMP积累增加27 +/- 8%。在百日咳毒素处理的细胞中,长期用乙醇治疗并没有进一步增强PGE1的刺激。这些结果表明,功能Gi是毒蕈碱胆碱能诱导的pge1刺激的cAMP积累增强的发展所必需的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Muscarinic cholinergic receptor-induced enhancement of PGE1-stimulated cAMP accumulation in neuroblastoma X glioma cells: prevention by pertussis toxin.

Chronic treatment of neuroblastoma X glioma hybrid cells (NG 108-15) with the muscarinic cholinergic agonist carbachol, which acutely inhibits adenylate cyclase, resulted in a 104 +/- 10% increase in PGE1-stimulated cAMP accumulation. Pretreatment of intact cells with pertussis toxin can structurally modify the inhibitory regulatory protein, Gi, by ADP-ribosylation and thus abolish the acute inhibition by carbachol. Pretreatment of the cells with pertussis toxin also resulted in a 27 +/- 8% increase in PGE1-stimulated cAMP accumulation. In the pertussis toxin-treated cells, chronic treatment with carbachol did not further enhance the PGE1 stimulation. These results suggest that functional Gi is required for the development of muscarinic cholinergic-induced enhancement of PGE1-stimulated cAMP accumulation.

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