Key result
Disruption of microtubule transport with nocodazole increased A-type potassium current densities from 20.9 to 34.0 pA/pF in rat ventricular myocytes.
Effect estimate: 1.6-fold increase
Absolute Event Rate: 34% vs 20.9%
The regulation of cardiac potassium channel surface expression involves a common dynein-dependent process operating similarly on various channels.
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Dynein-microtubule transport shapes cardiac K+ channel expression in vitro; leaves open relevance to disease remodeling.
Loewen et al. (2008) studied this question. Microtubule transport disruption (nocodazole or p50 overexpression) vs. Control cells was evaluated on A-type potassium current density at +90 mV (1.6-fold increase). Disruption of microtubule transport with nocodazole increased A-type potassium current densities from 20.9 to 34.0 pA/pF in rat ventricular myocytes.
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