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Sci. Signal., 2 August 2011
Vol. 4, Issue 184, p. pe35
[DOI: 10.1126/scisignal.2002225]

PERSPECTIVES

K2P Potassium Channels, Mysterious and Paradoxically Exciting

Steve A. N. Goldstein*

Department of Pediatrics and Institute for Molecular Pediatric Sciences, University of Chicago, Chicago, IL 60615, USA.

Abstract: New evidence reveals that the common electrolyte disorder hypokalemia can induce K2P1 channels that are normally selective for K+ to break the rules and conduct Na+. This defiant behavior leads to paradoxical depolarization of many cells in the heart, increasing the risk for lethal arrhythmia. The new research resolves a mystery uncovered 50 years ago and bestows an array of new riddles. Here, I discuss how K2P1 might achieve this alchemy—through stable residence of the K+ selectivity filter in a Na+-conductive state between its open and C-inactive configurations—and predict that other K+ channels and environmental stimuli will be discovered to produce the same excitatory misconduct.

* Corresponding author. E-mail: sangoldstein{at}uchicago.edu; goldstein{at}brandeis.edu

Citation: S. A. N. Goldstein, K2P Potassium Channels, Mysterious and Paradoxically Exciting. Sci. Signal. 4, pe35 (2011).

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SUMOylation Silences Heterodimeric TASK Potassium Channels Containing K2P1 Subunits in Cerebellar Granule Neurons.
L. D. Plant, L. Zuniga, D. Araki, J. D. Marks, and S. A. N. Goldstein (2012)
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Acid-sensitive TWIK and TASK Two-pore Domain Potassium Channels Change Ion Selectivity and Become Permeable to Sodium in Extracellular Acidification.
L. Ma, X. Zhang, M. Zhou, and H. Chen (2012)
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