期刊
FEBS LETTERS
卷 486, 期 3, 页码 310-314出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/S0014-5793(00)02298-5
关键词
isoproterenol; cAMP; protein kinase A; mammalian target of rapamycin; lung
资金
- NHLBI NIH HHS [HL-09806, HL-48129] Funding Source: Medline
We studied whether the beta -adrenergic agonist, isoproterenol (ISO), regulates Na,K-ATPase in alveolar epithelial cells (AEC) via a mitogen-activated protein kinase (MAPK)/ extracellular signaling related kinase (ERK) dependent pathway. ISO increased ERK activity in AEC by 10 min via a beta -adrenergic receptor, protein kinase A (PKA)-dependent mechanism. Activation of the MAPK pathway by ISO, resulted in increased Na,K-ATPase beta 1and alpha1 subunit protein abundance in whole cell lysates, which resulted in functional Na,K-ATPases at the basolateral membranes. ISO did not change the alpha1 or beta1 mRNA steady state levels, but rapamycin, the inhibitor of the mammalian target of rapamycin, also blocked the ISO-mediated increase in Na,K-ATPase total protein abundance, suggesting a posttranscriptional regulation. We conclude that ISO, regulates the Na,K-ATPase in AEC via PKA, ERK and rapamycin-sensitive mechanisms. (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据