October 19, 2013Journal of Biological ChemistryOpen Access

Ca2+ Elevation and Oxidative Stress Induce KCNQ1 Protein Translocation from the Cytosol to the Cell Surface and Increase Slow Delayed Rectifier (IKs) in Cardiac Myocytes

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Population

Cardiac myocytes (ventricular myocytes)

Design

Preclinical

Authors

YWYuhong WangUniversity of Shanghai for Science and Technology DZDimitar P. ZankovNational Cerebral and Cardiovascular Center MJMin JiangElectrophysiology

Discussion

Member takes

Implication

May enhance repolarization reserve under stress in animal myocytes; leaves open translation to human arrhythmias or therapies.

Structured PICO

Population

Cardiac myocytes (ventricular myocytes)

Intervention

Stress conditions ([Ca2+]i elevation, oxidative overload, or AT1R stimulation)

Outcome

KCNQ1 distribution and KCNQ1/KCNE1 colocalizationsurrogate

Stressful conditions increase IKs by inducing KCNQ1 movement to the cell surface, representing a mechanism for repolarization reserve in ventricular myocytes.

Cite This Study

Wang et al. (2013) studied this question.

synapsesocial.com/papers/6a76925f4ea07eb233cff369 https://doi.org/10.1074/jbc.m113.504746

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Ca2+ Elevation and Oxidative Stress Induce KCNQ1 Protein Translocation from the Cytosol to the Cell Surface and Increase Slow Delayed Rectifier (IKs) in Cardiac Myocytes

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Ca2+ Elevation and Oxidative Stress Induce KCNQ1 Protein Translocation from the Cytosol to the Cell Surface and Increase Slow Delayed Rectifier (IKs) in Cardiac Myocytes

Discussion

Member takes

Implication

Structured PICO

Cite This Study

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