Atrial fibrillation-associated minK38G/S polymorphism modulates delayed rectifier current and membrane localization
Population
Chinese hamster ovary cells, COS-7 cells, and computer simulations with a human atrial action potential model
Comparison
Expression of the minK38G isoform vs Expression of the minK38S isoform
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Hypothesis-generating for minK38G in AF; leaves open whether reduced I(Ks) drives clinical arrhythmia risk.
Structured PICO
P
Population
Chinese hamster ovary (CHO) cells, COS-7 cells, and computer simulations with a human atrial action potential model
I
Intervention
Expression of the minK38G isoform (co-expressed with KvLQT1 or HERG)
C
Comparator
Expression of the minK38S isoform
O
Outcome
Density of slow delayed rectifier current (I(Ks)), I(Ks) kinetics, voltage-dependence, and KvLQT1 membrane localizationsurrogate
The minK38G polymorphism associated with atrial fibrillation reduces I(Ks) density, likely due to decreased KvLQT1 membrane expression, providing a potential mechanism for its arrhythmogenic effect.
Cite This Study
Ehrlich et al. (2005) studied this question.