December 1, 2000Journal of NeuroscienceOpen Access

The Human Skeletal Muscle Na Channel Mutation R669H Associated with Hypokalemic Periodic Paralysis Enhances Slow Inactivation

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Population

Human embryonic kidney cells expressing the hSkM1-R669H mutant Na channel

Design

Preclinical

Authors

ASArie StruykGwynedd Mercy University KSKylie A. ScogganHealth Canada DBDennis E. BulmanUniversity of Alberta

Discussion

Member takes

Implication

May prolong weakness episodes in hypokalemic periodic paralysis; hypothesis-generating for mechanism-based therapies pending human data.

Structured PICO

Population

Human embryonic kidney cells expressing the hSkM1-R669H mutant Na channel

Intervention

hSkM1-R669H mutation

Outcome

Gating properties (activation, fast inactivation, and slow inactivation)surrogate

The R669H mutation in the human skeletal muscle Na channel enhances slow inactivation, which may contribute to prolonged attacks of weakness in hypokalemic periodic paralysis.

Cite This Study

Struyk et al. (2000) studied this question.

synapsesocial.com/papers/6a707f533ce530166bc2d895 https://doi.org/10.1523/jneurosci.20-23-08610.2000

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The Human Skeletal Muscle Na Channel Mutation R669H Associated with Hypokalemic Periodic Paralysis Enhances Slow Inactivation

Discussion

Member takes

Implication

Structured PICO

Cite This Study

The Human Skeletal Muscle Na Channel Mutation R669H Associated with Hypokalemic Periodic Paralysis Enhances Slow Inactivation

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider