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- W2000871227 endingPage "1380" @default.
- W2000871227 startingPage "1357" @default.
- W2000871227 abstract "In cardiac muscle, the sarcolemmal sodium/potassium ATPase is the principal quantitative means of active transport at the myocyte cell surface, and its activity is essential for maintaining the trans-sarcolemmal sodium gradient that drives ion exchange and transport processes that are critical for cardiac function. The 72-residue phosphoprotein phospholemman regulates the sodium pump in the heart: unphosphorylated phospholemman inhibits the pump, and phospholemman phosphorylation increases pump activity. Phospholemman is subject to a remarkable plethora of post-translational modifications for such a small protein: the combination of three phosphorylation sites, two palmitoylation sites, and one glutathionylation site means that phospholemman integrates multiple signaling events to control the cardiac sodium pump. Since misregulation of cytosolic sodium contributes to contractile and metabolic dysfunction during cardiac failure, a complete understanding of the mechanisms that control the cardiac sodium pump is vital. This review explores our current understanding of these mechanisms." @default.
- W2000871227 created "2016-06-24" @default.
- W2000871227 creator A5015636183 @default.
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- W2000871227 creator A5045146259 @default.
- W2000871227 creator A5067134785 @default.
- W2000871227 creator A5090338124 @default.
- W2000871227 date "2012-09-07" @default.
- W2000871227 modified "2023-10-16" @default.
- W2000871227 title "Regulation of the cardiac sodium pump" @default.
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