April 13, 2004AJP Heart and Circulatory Physiology
Pharmacological rescue of trafficking defective HERG channels formed by coassembly of wild-type and long QT mutant N470D subunits
Why the study?
Does E-4031 improve cell surface expression of trafficking defective HERG channels formed by coassembly of wild-type and N470D subunits?
Population
Cells expressing HERG N470D mutant and wild-type subunits
Comparison
E-4031 (HERG channel blocking drug) vs Control (cells not cultured in E-4031)
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Supports E-4031 as trafficking corrector in LQT2 models; altered phenotype leaves functional rescue and clinical translation open.
Structured PICO
Does E-4031 improve cell surface expression of trafficking defective HERG channels formed by coassembly of wild-type and N470D subunits?
P
Population
Cells expressing HERG N470D mutant and wild-type subunits
I
Intervention
E-4031 (HERG channel blocking drug)
C
Comparator
Control (cells not cultured in E-4031)
O
Outcome
Cell surface expression of heteromeric channels and electrophysiological phenotypesurrogate
The HERG channel blocker E-4031 can pharmacologically rescue the trafficking defect of heteromeric channels formed by wild-type and long QT mutant N470D subunits.
Cite This Study
Gong et al. (2004) studied this question.