June 10, 2009Biochemical and Biophysical Research CommunicationsOpen Access

hERG1a/1b heteromeric currents exhibit amplified attenuation of inactivation in variant 1 short QT syndrome

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Population

Co-expressed hERG1a/1b channels (in vitro model)

Comparison

N588K mutation vs hERG1a expressed alone

Design

Preclinical

Authors

MMM.J. McPate HZHuiyuan ZhangSichuan University JCJonathan M. CordeiroUniversidad Complutense de Madrid

Discussion

Member takes

Implication

Supports heteromeric hERG models for mutation studies; leaves open clinical translation to arrhythmia risk.

Structured PICO

Population

Co-expressed hERG1a/1b channels (in vitro model)

Intervention

N588K mutation (gain-of-function, responsible for SQT1 variant of short QT syndrome)

Comparator

hERG1a expressed alone

Outcome

Electrophysiological effects on current (I(hERG1a/1b)) including activation, deactivation, and inactivationsurrogate

The N588K mutation causes amplified attenuation of inactivation in co-expressed hERG1a/1b channels, indicating that heteromeric channels should be used when investigating hERG mutations.

Cite This Study

McPate et al. (2009) studied this question.

synapsesocial.com/papers/6a912d02ae2c4ed52ef124ca https://doi.org/10.1016/j.bbrc.2009.05.134

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hERG1a/1b heteromeric currents exhibit amplified attenuation of inactivation in variant 1 short QT syndrome

Discussion

Member takes

Implication

Structured PICO

Cite This Study

hERG1a/1b heteromeric currents exhibit amplified attenuation of inactivation in variant 1 short QT syndrome

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider