ArticleCellular and molecular life sciences : CMLS2010
Dependence of 6beta-acetoxy-7alpha-hydroxyroyleanone block of Kv1.2 channels on C-type inactivation.
Article in Cellular and molecular life sciences : CMLS, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 11 citations in OpenAlex.
- Voltage-gated KChinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2018Article
- Role of voltage-gated K(+) channels in regulating Ca(2+) entry in rat cortical astrocytes.The journal of physiological sciences : JPS · 2015Article
- Control of ionic selectivity by a pore helix residue in the Kv1.2 channel.The journal of physiological sciences : JPS · 2010Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
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Abstract
Voltage-gated K(+) (Kv) channels exhibit slow or C-type inactivation during continuous depolarization. A selective pharmacological agent targeting C-type inactivation is hitherto lacking. Here, we report that 6beta-acetoxy-7alpha-hydroxyroyleanone (AHR), a diterpenoid compound isolated from Taiwania cryptomerioides, can selectively modify C-type inactivation of Kv1.2 channels. Extracellular, but not intracellular, AHR (50 muM) dramatically accelerated the slow decay of Kv currents and left-shifted the steady-state inactivation curve. AHR blocked Kv currents with an IC(50) of 17.7 muM. AHR did not affect the kinetics and voltage-dependence of Kv1.2 channel activation. Channel block by AHR was independent of intracellular K(+) concentration. In addition, effect of AHR was much attenuated in a Kv1.2 V370G mutant defective in C-type inactivation. Therefore, block of Kv1.2 channels by AHR did not appear to involve direct occlusion of the outer pore but depended on C-type inactivation. AHR could thus be a probe targeting Kv channel C-type inactivation gate.
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