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Deletion in mice of X-linked, Brugada syndrome- and atrial fibrillation-associated Kcne5 augments ventricular K_V currents and predisposes to ventricular arrhythmia.

ABSTRACT: KCNE5 is an X-linked gene encoding KCNE5, an ancillary subunit to voltage-gated potassium (K_V) channels. Human KCNE5 mutations are associated with atrial fibrillation (AF)- and Brugada syndrome (BrS)-induced cardiac arrhythmias that can arise from increased potassium current in cardiomyocytes. Seeking to establish underlying molecular mechanisms, we created and studied Kcne5 knockout ( Kcne5^-/0) mice. Intracardiac ECG revealed that Kcne5 deletion caused ventricular premature beats, increased susceptibility to induction of polymorphic ventricular tachycardia (60 vs. 24% in Kcne5^+/0 mice), and 10% shorter ventricular refractory period. Kcne5 deletion increased mean ventricular myocyte K_V current density in the apex and also in the subpopulation of

SUBMITTER: David JP

PROVIDER: S-EPMC6338634 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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Deletion in mice of X-linked, Brugada syndrome- and atrial fibrillation-associated Kcne5 augments ventricular K_V currents and predisposes to ventricular arrhythmia.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Deletion in mice of X-linked, Brugada syndrome- and atrial fibrillation-associated Kcne5 augments ventricular KV currents and predisposes to ventricular arrhythmia.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Deletion in mice of X-linked, Brugada syndrome- and atrial fibrillation-associated Kcne5 augments ventricular K_V currents and predisposes to ventricular arrhythmia.