The alpha 2L111R,N122D isoform of the Na,K-ATPase expressed in HeLa cells does not undergo an adipocyte-like increase in activity in response to insulin

被引:3
作者
Coppi, MV
Guidotti, G
机构
[1] Dept. of Molec. and Cellular Biology, Harvard University, Cambridge, MA 02138
关键词
D O I
10.1006/bbrc.1997.6981
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In the rat adipocyte, insulin increases potassium uptake by a preferential activation of the alpha 2 isoform of the Na,K-ATPase. The question under consideration here is whether expression of the alpha 2 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 alpha 1 and alpha 2RD (alpha 2L111R,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 Rb-86(+)/K+ uptake by the ouabain resistant rat alpha 1 and rat alpha 2RD subunits. We conclude that the mechanism of insulin activation of the alpha 2RD isoform in HeLa cells differs from that of the wild type alpha 2 isoform in the rat adipocyte. (C) 1997 Academic Press.
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页码:444 / 448
页数:5
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