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- W2029194434 abstract "Resveratrol (REV) is a naturally occurring phytoalexin that inhibits neuronal K + channels; however, the molecular mechanisms behind the effects of REV and the relevant α-subunit are not well defined. With the use of patch-clamp technique, cultured cerebellar granule cells, and HEK-293 cells transfected with the K v 2.1 and K v 2.2 α-subunits, we investigated the effect of REV on K v 2.1 and K v 2.2 α-subunits. Our data demonstrated that REV significantly suppressed K v 2.2 but not K v 2.1 currents with a fast, reversible, and mildly concentration-dependent manner and shifted the activation or inactivation curve of K v 2.2 channels. Activating or inhibiting the cAMP/PKA pathway did not abolish the inhibition of K v 2.2 current by REV. In contrast, activation of PKC with phorbol 12-myristate 13-acetate mimicked the inhibitory effect of REV on K v 2.2 by modifying the activation or inactivation properties of K v 2.2 channels and eliminated any further inhibition by REV. PKC and PKC-α inhibitor completely eliminated the REV-induced inhibition of K v 2.2. Moreover, the effect of REV on K v 2.2 was reduced by preincubation with antagonists of GPR30 receptor and shRNA for GPR30 receptor. Western blotting results indicated that the levels of PKC-α and PKC-β were significantly increased in response to REV application. Our data reveal, for the first time, that REV inhibited K v 2.2 currents through PKC-dependent pathways and a nongenomic action of the oestrogen receptor GPR30." @default.
- W2029194434 created "2016-06-24" @default.
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- W2029194434 date "2013-09-01" @default.
- W2029194434 modified "2023-10-02" @default.
- W2029194434 title "Resveratrol inhibits K<sub>v</sub>2.2 currents through the estrogen receptor GPR30-mediated PKC pathway" @default.
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- W2029194434 doi "https://doi.org/10.1152/ajpcell.00146.2013" @default.
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