Key result
The zebrafish reggae mutation in the zERG potassium channel causes premature channel activation and defective inactivation, resulting in shortened QT intervals and accelerated cardiac repolarization.
Population
Zebrafish mutation reggae (reg) embryos and adult zebrafish
Comparison
Genetic and pharmacological inhibition of zERG vs Wild-type zebrafish
Design
Preclinical
Authors
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Provides first zebrafish model for short-QT syndrome; leaves open human translation and therapeutic implications.
The zebrafish reggae mutant represents the first animal model for human short-QT syndrome, demonstrating that a gain-of-function mutation in the zERG potassium channel accelerates cardiac repolarization.
Hassel et al. (2008) studied Short-QT syndrome. reggae (reg) mutation in the zERG potassium channel vs. Wild-type zebrafish was evaluated on QT intervals and cardiac repolarization. The zebrafish reggae mutation in the zERG potassium channel causes premature channel activation and defective inactivation, resulting in shortened QT intervals and accelerated cardiac repolarization.
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