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• W2016042137 abstract "In humans, Kv1.5 (hKv1.5) channels conduct the ultra-rapid delayed rectifier K+ current (IKur) that is important for the repolarization of cardiac action potentials. We aimed at examining the effect of lipoxygenase inhibitors cinnamyl-3,4-dihydroxy-α-cyanocinnamate (CDC), nordihydroguaiaretic acid (NDGA), and gossypol on hKv1.5 wild-type and mutant channels heterologously expressed in Chinese hamster ovary (CHO) cells, by use of the site-directed mutagenesis and whole-cell patch-clamp method. CDC and NDGA, but not gossypol, a structurally dissimilar inhibitor, reversibly inhibited hKv1.5 current in a concentration-dependent manner with IC50 of 5.7 μM and 16.4 μM, respectively. The blockade evoked by both drugs was voltage-dependent between − 20 and + 10 mV (voltage range of channel opening). Moreover, this blocking action was found to progress with time during depolarizing voltage steps with a more rapid block at higher concentrations. CDC induced slight but significant delay of the deactivation rate. However, NDGA markedly slowed the deactivation time course, resulting in a tail crossover phenomenon. The recovery time constants from current block at repolarizing potentials for CDC and NDGA were 60.9 ms and 129.7 ms, respectively. Mutation of arginine 487 to valine (R487V) in the outer pore region of the channel significantly reduced the CDC action. These results demonstrate for the first time that CDC and NDGA block hKv1.5 channels by binding to the open state of the channels, independently of their effects on lipoxygenase activity. The putative binding site for CDC appears to be related to arginine 487 located in the outer pore region." @default.
• W2016042137 created "2016-06-24" @default.
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• W2016042137 date "2008-12-01" @default.
• W2016042137 modified "2023-10-14" @default.
• W2016042137 title "Cinnamyl-3,4-dihydroxy-α-cyanocinnamate and nordihydroguaiaretic acid inhibit human Kv1.5 currents independently of lipoxygenase" @default.
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• W2016042137 doi "https://doi.org/10.1016/j.ejphar.2008.10.010" @default.
• W2016042137 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18930721" @default.
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