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June 25, 2007The Journal of General PhysiologyOpen Access

Do Hyperpolarization-induced Proton Currents Contribute to the Pathogenesis of Hypokalemic Periodic Paralysis, a Voltage Sensor Channelopathy?

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Editorial

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KJKarin Jurkat‐RottUniversität Ulm FLFrank Lehmann‐HornUniversität Ulm

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Implication

This editorial discusses the pathophysiological mechanisms of hypokalemic periodic paralysis, a voltage sensor channelopathy.

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Key points are not available for this paper at this time.

Cite This Study

Jurkat‐Rott et al. (2007) studied this question.

synapsesocial.com/papers/6a7dee4f6ef7ec97ba7d922c https://doi.org/10.1085/jgp.200709834

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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1Voltage-sensor sodium channel mutations cause hypokalemic periodic paralysis type 2 by enhanced inactivation and reduced current2000 · 266 citations
2A Na+ Channel Mutation Linked to Hypokalemic Periodic Paralysis Exposes a Proton-selective Gating Pore2007 · 171 citations
3Enhanced inactivation and pH sensitivity of Na+ channel mutations causing hypokalaemic periodic paralysis type II2002 · 78 citations
4The Human Skeletal Muscle Na Channel Mutation R669H Associated with Hypokalemic Periodic Paralysis Enhances Slow Inactivation2000 · 94 citations
5Insulin acts in hypokalemic periodic paralysis by reducing inward rectifier K current1999 · 113 citations