Population
In vitro cell model expressing KvLQT1 and minK mutants (minK-L51H and minK-ER)
Comparison
Expression of minK-L51H or minK-ER vs Wild-type (WT) minK/KvLQT1 or KvLQT1 without minK
Design
Preclinical
Authors
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MinK-L51H trafficking defect may contribute to LQT5; leaves open clinical translation and therapeutic implications.
This study demonstrates that a minK LQT mutation (minK-L51H) causes trafficking defects in its associated alpha-subunit (KvLQT1), leading to decreased I(Ks) current.
Krumerman et al. (2004) studied this question.
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