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H-35肝癌细胞中ATP诱导的钙动员和肌醇1,4,5-三磷酸的形成

ATP-induced calcium mobilization and inositol 1,4,5-triphosphate formation in H-35 hepatoma cells.

作者信息

Horstman D A, Tennes K A, Putney J W

出版信息

FEBS Lett. 1986 Aug 18;204(2):189-92. doi: 10.1016/0014-5793(86)80809-2.

Abstract

Addition of ATP (but not epinephrine, angiotensin II, vasopressin, or platelet-activating factor) to H-35 hepatoma cells whose cellular lipids have been pre-labelled with [3H]inositol, causes a rapid increase in [3H]inositol triphosphate. In H-35 cells pre-incubated in the presence of 45Ca2+, ATP causes a similarly rapid release of 45Ca2+. The concentration-effect relationships for inositol triphosphate formation and Ca2+ efflux are similar to those reported previously for differentiated hepatocytes. These results demonstrate that at least one of the Ca2+-mobilizing receptors normally found on hepatocytes is functionally retained in the H-35 hepatoma cell line and thus could provide a useful model for the study of these receptor mechanisms in liver.

摘要

将ATP(而非肾上腺素、血管紧张素II、血管加压素或血小板活化因子)添加到细胞脂质已用[3H]肌醇预标记的H-35肝癌细胞中,会导致[3H]肌醇三磷酸迅速增加。在45Ca2+存在下预孵育的H-35细胞中,ATP会引起类似的45Ca2+快速释放。肌醇三磷酸形成和Ca2+流出的浓度-效应关系与先前报道的分化肝细胞的关系相似。这些结果表明,肝细胞上正常存在的至少一种Ca2+动员受体在功能上保留在H-35肝癌细胞系中,因此可为研究肝脏中的这些受体机制提供有用的模型。

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