RETRACTED: Increased Activation of the TRESK K+ Mediates Vago-Vagal Reflex Malfunction in Diabetic Rats
G Grabauskas, X Wu, I Song, SY Zhou, T Lanigan… - 2016 - Elsevier
G Grabauskas, X Wu, I Song, SY Zhou, T Lanigan, C Owyang
2016•ElsevierIt has already been reported that short ionomycin application can mediate fully reversible
effects that could be repeatedly induced (Yoshida and Plant, 1992). Among Ca2+-
associated K2P channels, TRESK is unique because TRESK channels are activated by
elevations in the cytoplasmic Ca2+ concentration via dephosphorylation by calcineurin,
whereas other Ca2+-associated K2P channels, TREK and TASK, are suppressed by Ca2+
via PKC pathways (Czirják and Enyedi, 2006; Enyedi and Czirják, 2010; Grabauskas et al …
effects that could be repeatedly induced (Yoshida and Plant, 1992). Among Ca2+-
associated K2P channels, TRESK is unique because TRESK channels are activated by
elevations in the cytoplasmic Ca2+ concentration via dephosphorylation by calcineurin,
whereas other Ca2+-associated K2P channels, TREK and TASK, are suppressed by Ca2+
via PKC pathways (Czirják and Enyedi, 2006; Enyedi and Czirják, 2010; Grabauskas et al …
It has already been reported that short ionomycin application can mediate fully reversible effects that could be repeatedly induced (Yoshida and Plant, 1992). Among Ca2+-associated K2P channels, TRESK is unique because TRESK channels are activated by elevations in the cytoplasmic Ca2+ concentration via dephosphorylation by calcineurin, whereas other Ca2+-associated K2P channels, TREK and TASK, are suppressed by Ca2+ via PKC pathways (Czirják and Enyedi, 2006; Enyedi and Czirják, 2010; Grabauskas et al., 2016). Thus, the Ca2+-dependent induction of DShI in combination with the complete blockade of DShI by the calcineurin inhibitor FK506 is an additional strong argument for TRESK mediating DShI.
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