Abstract
Heart disease remains the leading cause of death worldwide. Small-conductance Ca2+-activated K+ (SK) channels are unique in that they are gated solely by changes in intracellular Ca2+ and are upregulated in heart failure and atrial fibrillation. The possible roles of SK channels in cardiac arrhythmias are increasingly being recognized. One important contributor to SK channel regulation is calmodulin (CaM), which activates SK channels upon binding by Ca2+. In addition, phosphatidylinositol 4,5-bisphosphate (PIP2), a phospholipid in the cell membrane, has been suggested to modulate the activation of SK channels.
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