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Activation of P2Y2 purinoceptor inhibits the activity of the Na+/K+-ATPase in HeLa cells

机译:P2Y2嘌呤受体的激活抑制HeLa细胞中Na + / K + -ATPase的活性

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The role of ATP on regulation of the Na+/K+-ATPase activity in the human cancerous HeLa cells was investigated. HeLa cells stimulated with increasing ATP concentrations showed a dose-dependent inhibition of the Na+/K+-ATPase activity. These effects were also obtained by UTP. ATP and UTP provoked a rise in intracellular calcium concentration ([Ca2+](i)) persisting for at least 4 min. The inhibitor of phospholipase C, U73122, blocked the elevation of [Ca2+](i) provoked by ATP/UTP. The expression of mRNA for P2Y2 and P2Y6 receptors was demonstrated by RTPCR. ATP/UTP activated PKC-alpha, -betaI and -epsilon isoforms, but not PKC-delta and -zeta. The inhibition of the Na+/K+-ATPase activity by ATP/UTP was blocked by Go6976, a specific inhibitor of the calcium-dependent PKCs. In conclusion, our results suggest that ATP/UTP modulate Na+/K+-ATPase activity in HeLa cells through the P2Y2 purinoceptor via calcium mobilisation and activation of calcium-dependent PKCs. (C) 2002 Elsevier Science Inc. All rights reserved. [References: 50]
机译:研究了ATP在调节人癌HeLa细胞中Na + / K + -ATPase活性中的作用。 ATP浓度增加刺激的HeLa细胞显示出Na + / K + -ATPase活性的剂量依赖性抑制。这些效果也是通过UTP获得的。 ATP和UTP引起细胞内钙浓度([Ca2 +](i))升高至少持续4分钟。磷脂酶C的抑制剂U73122阻止了ATP / UTP引起的[Ca2 +](i)升高。 RTPCR证实了P2Y2和P2Y6受体的mRNA表达。 ATP / UTP激活PKC-alpha,-betaI和-epsilon同种型,但不激活PKC-delta和-zeta。 ATP / UTP对Na + / K + -ATPase活性的抑制被钙依赖性PKC的特异性抑制剂Go6976阻断。总之,我们的结果表明,ATP / UTP通过P2Y2嘌呤受体通过钙动员和钙依赖性PKCs活化来调节HeLa细胞中的Na + / K + -ATPase活性。 (C)2002 Elsevier Science Inc.保留所有权利。 [参考:50]

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