Suppr超能文献

细胞肿胀触发的蛋白激酶信号通路,参与分离的大鼠肝细胞中糖原合酶和乙酰辅酶A羧化酶的激活。

Protein kinase signaling pathway triggered by cell swelling and involved in the activation of glycogen synthase and acetyl-CoA carboxylase in isolated rat hepatocytes.

作者信息

Krause U, Rider M H, Hue L

机构信息

Hormone and Metabolic Research Unit, University of Louvain Medical School, and International Institute of Cellular and Molecular Pathology, B-1200 Brussels, Belgium.

出版信息

J Biol Chem. 1996 Jul 12;271(28):16668-73. doi: 10.1074/jbc.271.28.16668.

Abstract

Incubation of isolated hepatocytes with glutamine or proline or in hypotonic media is known to activate glycogen synthase and acetyl-CoA carboxylase as a result of cell swelling. We report here that the same experimental conditions caused an activation of phosphatidylinositol 3-kinase and p70 ribosomal protein S6 kinase (p70 S6 kinase) but did not modify the activity of p42 mitogen-activated protein kinase. In addition, rapamycin, an inhibitor of p70 S6 kinase activation, prevented the amino acid- and hypotonicity-induced activation of p70 S6 kinase but did not block the activation of glycogen synthase and acetyl-CoA carboxylase, thus ruling out p70 S6 kinase as a necessary component in the activation pathway. By contrast, wortmannin or LY294002, inhibitors of phosphatidylinositol 3-kinase, completely blocked the activation of phosphatidylinositol 3-kinase and p70 S6 kinase and partly blocked the activation of glycogen synthase and acetyl-CoA carboxylase. Therefore, phosphatidylinositol 3-kinase might be a component of the signaling pathway that is triggered by cell swelling and is responsible, at least in part, for the activation of glycogen synthase and acetyl-CoA carboxylase. Incubation of hepatocytes with 0.1 microM epidermal growth factor doubled the activity of p42 mitogen-activated protein kinase without activating glycogen synthase.

摘要

已知将分离的肝细胞与谷氨酰胺或脯氨酸一起孵育,或在低渗培养基中孵育,会因细胞肿胀而激活糖原合酶和乙酰辅酶A羧化酶。我们在此报告,相同的实验条件会导致磷脂酰肌醇3激酶和p70核糖体蛋白S6激酶(p70 S6激酶)的激活,但不会改变p42丝裂原活化蛋白激酶的活性。此外,雷帕霉素是一种p70 S6激酶激活抑制剂,可阻止氨基酸和低渗诱导的p70 S6激酶激活,但不会阻断糖原合酶和乙酰辅酶A羧化酶的激活,因此排除了p70 S6激酶是激活途径中必需成分的可能性。相比之下,磷脂酰肌醇3激酶抑制剂渥曼青霉素或LY294002可完全阻断磷脂酰肌醇3激酶和p70 S6激酶的激活,并部分阻断糖原合酶和乙酰辅酶A羧化酶的激活。因此,磷脂酰肌醇3激酶可能是由细胞肿胀触发的信号通路的一个组成部分,并且至少部分负责糖原合酶和乙酰辅酶A羧化酶的激活。用0.1微摩尔表皮生长因子孵育肝细胞可使p42丝裂原活化蛋白激酶的活性增加一倍,而不会激活糖原合酶。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验