期刊
CELLULAR AND MOLECULAR LIFE SCIENCES
卷 70, 期 8, 页码 1357-1380出版社
SPRINGER BASEL AG
DOI: 10.1007/s00018-012-1134-y
关键词
Sodium pump; Ion transport; Phospholemman; FXYD; Heart; Intracellular sodium; Protein kinase A; Protein kinase C; Palmitoylation
资金
- Medical Research Council [G0700903]
- British Heart Foundation [RG/07/001, PG/10/93/28650]
- British Heart Foundation [PG/12/6/29366, RG/12/4/29426, RG/07/001/22628, PG/10/93/28650] Funding Source: researchfish
- Medical Research Council [G0700903] Funding Source: researchfish
- MRC [G0700903] Funding Source: UKRI
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.
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