百日咳毒素对A-431人表皮样癌细胞p2 -嘌呤能受体信号转导的影响

Enzyme & protein Pub Date : 1994-01-01 DOI:10.1159/000474992
K Sugita, K Kurihara, K Hosoi, T Atsumi, T Takahashi, M Kohno, T Ueha
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引用次数: 4

摘要

在A-431细胞中,细胞外ATP刺激p2 -嘌呤能受体引起肌醇1,4,5-三磷酸(InsP3)的产生,随后从细胞内储存中动员Ca2+;细胞外液的Ca2+内流和磷脂酰胆碱(PtdCho)的分解也伴随着这种InsP3/Ca2+信号。当A-431细胞被百日咳毒素(PTX)预处理时,胞质中InsP3的产生和Ca2+的升高被强烈抑制。PTX对Ca2+内流也有抑制作用,但效果远弱于对InsP3/Ca2+升高的抑制作用。atp刺激的PtdCho分解未见抑制作用。这些结果表明,除了ptx敏感的g蛋白外,还有一个系统介导p2 -嘌呤能受体的功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of pertussis toxin on signal transductions via P2-purinergic receptors in A-431 human epidermoidal carcinoma cells.

In A-431 cells, stimulation of P2-purinergic receptors with extracellular ATP caused production of inositol 1,4,5-trisphosphate (InsP3), followed by mobilization of Ca2+ from intracellular stores; Ca2+ influx from the extracellular fluid and breakdown of phosphatidylcholine (PtdCho) also accompanied this InsP3/Ca2+ signalling. When A-431 cells were pretreated with pertussis toxin (PTX), production of InsP3 and elevation of cytosolic Ca2+ were strongly inhibited. PTX also inhibited the Ca2+ influx, but the effect was much weaker than that for InsP3/Ca2+ elevation. No inhibitory effect was observed in ATP-stimulated PtdCho breakdown. These results suggest that there is a system(s) which mediates the functions of P2-purinergic receptors in addition to PTX-sensitive G-proteins.

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