Key result
Coexpression of IsK and KvLQT1 subunits resulted in a 6-100 fold higher affinity for IKs blockers and dramatically enhanced steady-state currents with activators compared to KvLQT1 alone.
Population
KvLQT1 homopolymeric K+ channels and heteropolymeric IKs channels (coexpression of IsK and KvLQT1 subunits)
Comparison
IKs blockers and activators vs KvLQT1 homopolymeric channels vs heteropolymeric…
Design
Preclinical
Authors
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IsK coexpression alters IKs pharmacology in vitro; leaves open translation to native channels or clinical drug effects.
Effect estimate: 6-100 fold higher affinity
The IsK protein is crucial for modulating the pharmacological sensitivity of IKs channels to both blockers and activators, which has implications for drug specificity in cardiac tissue.
Büsch et al. (1997) studied IKs channel pharmacology. IKs blockers (293B, azimilide, 17-beta-oestradiol) and activators (mefenamic acid, DIDS) vs. KvLQT1 homopolymeric channels was evaluated on Channel affinity and response to blockers and activators (6-100 fold higher affinity). Coexpression of IsK and KvLQT1 subunits resulted in a 6-100 fold higher affinity for IKs blockers and dramatically enhanced steady-state currents with activators compared to KvLQT1 alone.
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