Key result
Expression of the cloned KvLQT1 gene elicits a rapidly activating, K+-selective outward current that is inhibited by clofilium and resembles I(Ks) when coexpressed with minK.
The cloning and functional characterization of KvLQT1 demonstrates its role as a voltage-gated potassium channel that, together with minK, forms the cardiac I(Ks) current, elucidating the molecular mechanism of long QT syndrome.
No takes yet. Share an insight, caveat, or question.
Links KvLQT1 to I(Ks) loss in LQTS; leaves open targeted therapies from animal models.
Yang et al. (1997) studied Long QT syndrome. KvLQT1 expression was evaluated on Functional expression and electrophysiological properties of KvLQT1. Expression of the cloned KvLQT1 gene elicits a rapidly activating, K+-selective outward current that is inhibited by clofilium and resembles I(Ks) when coexpressed with minK.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: