The inward rectification mechanism of the HERG cardiac potassium channel
- PMID: 8587608
- DOI: 10.1038/379833a0
The inward rectification mechanism of the HERG cardiac potassium channel
Abstract
A human genetic defect associated with 'long Q-T syndrome', an abnormality of cardiac rhythm involving the repolarization of the action potential, was recently found to lie in the HERG gene, which codes for a potassium channel. The HERG K+ channel is unusual in that it seems to have the architectural plan of the depolarization-activated K+ channel family (six putative transmembrane segments), yet it exhibits rectification like that of the inward-rectifying K+ channels, a family with different molecular structure (two transmembrane segments). We have studied HERG channels expressed in mammalian cells and find that this inward rectification arises from a rapid and voltage-dependent inactivation process that reduces conductance at positive voltages. The inactivation gating mechanism resembles that of C-type inactivation, often considered to be the 'slow inactivation' mechanism of other K+ channels. The characteristics of this gating suggest a specific role for this channel in the normal suppression of arrhythmias.
Comment in
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The inconstancy of the human heart.Nature. 1996 Feb 29;379(6568):767-8. doi: 10.1038/379767a0. Nature. 1996. PMID: 8587597 No abstract available.
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