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The alpha2L111R,N122D isoform of the Na,K-ATPase expressed in HeLa cells does not undergo an adipocyte-like increase in activity in response to insulin.

作者信息

Coppi M V, Guidotti G

机构信息

Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.

出版信息

Biochem Biophys Res Commun. 1997 Jul 18;236(2):444-8. doi: 10.1006/bbrc.1997.6981.

DOI:10.1006/bbrc.1997.6981
PMID:9240458
Abstract

In the rat adipocyte, insulin increases potassium uptake by a preferential activation of the alpha2 isoform of the Na,K-ATPase. The question under consideration here is whether expression of the alpha2 isoform is sufficient to replicate its differential activation by insulin. Accordingly, we compared the effect of insulin on the activity of the ouabain resistant rat alpha1 and alpha2RD (alpha2L111R,N122D) isoforms in HeLa cells. In HeLa cells, in contrast to the rat adipocyte, insulin produces an increase of equal magnitude in the rate of 86Rb+/K+ uptake by the ouabain resistant rat alpha1 and rat alpha2RD subunits. We conclude that the mechanism of insulin activation of the alpha2RD isoform in HeLa cells differs from that of the wild type alpha2 isoform in the rat adipocyte.

摘要

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