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首页> 外文期刊>Cellular Signalling >Evidence for transduction of mu but not kappa opioid modulation of extracellular signal-regulated kinase activity by G(z) and G(12) proteins
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Evidence for transduction of mu but not kappa opioid modulation of extracellular signal-regulated kinase activity by G(z) and G(12) proteins

机译：通过G（z）和G（12）蛋白转导mu但不是κ阿片类药物调节细胞外信号调节激酶活性的证据

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Chronic treatment with mu or kappa opioid agonists (greater than or equal to 2. h) inhibits EGF-induced ERK activation in opioid receptor overexpressing COS-7 cells. Although acute mu and kappa opioids activate ERK via a pertussis toxin-sensitive G protein, pertussis toxin insensitivity of the chronic mu (but not kappa) action was observed. Here, we tested several pertussis toxin-insensitive G proteins as candidates to transduce acute and/or chronic opioid modulation of ERK. Overexpressed G alpha(z) (but not G alpha(12)) transduced acute mu (but not kappa) ERK activation in pertussis toxin-treated COS-7 cells. Chronic mu (but not kappa) inhibited EGF stimulation of ERK in pertussis toxin-treated cells overexpressing G alpha(z), or G alpha(12). Transfection of G alpha(13) or G alpha(q) blocked inhibition under the same conditions. Overexpressed interfering and non-interfering G alpha(z) mutants differentially affected mu inhibition of ERK consistent with G(z) transduction. In this and prior studies, G alpha(z) and G alpha(12) immunoreactivity were detected in untransfected COS-7 cells, suggesting that these G proteins may be endogenous mediators of chronic mu inhibitory actions on ERK. (C) 2000 Elsevier Science Inc. All rights reserved. [References: 59]
机译：使用mu或kappa类阿片激动剂（大于或等于2. h）进行长期治疗，可抑制过表达阿片受体的COS-7细胞中EGF诱导的ERK活化。尽管急性mu和kappa类阿片类药物通过百日咳毒素敏感的G蛋白激活ERK，但仍观察到慢性mu（而非kappa）作用对百日咳毒素不敏感。在这里，我们测试了几种百日咳毒素不敏感的G蛋白，作为转导ERK的急性和/或慢性阿片样物质调节的候选药物。百日咳毒素治疗的COS-7细胞中过表达的G alpha（z）（但不是G alpha（12））转导了急性mu（但不是kappa）ERK激活。慢性mu（但不是kappa）抑制过表达Galpha（z）或Galpha（12）的经百日咳毒素处理的细胞中ERK对ERK的刺激。 G alpha（13）或G alpha（q）的转染在相同条件下阻断了抑制作用。过表达的干扰和非干扰G alpha（z）突变体差异影响mu抑制ERK与G（z）转导一致。在本研究和先前的研究中，在未转染的COS-7细胞中检测到G alpha（z）和G alpha（12）免疫反应性，表明这些G蛋白可能是对ERK的慢性mu抑制作用的内源性介质。 （C）2000 Elsevier Science Inc.保留所有权利。 [参考：59]

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