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Reactive Oxygen Species activates KCNH2. 9 / 9
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"The ROS scavenger N-acetyl cysteine (NAC) significantly attenuated hERG reduction induced by THIO and abolished the upregulation of ER stress marker proteins."
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"Recent evidence has shown that ROS can specifically modulate the function of HERG K + channels [58] : an enhancement of ROS production increases HERG outward K + currents, whereas a decrease in ROS le[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"We consider this highly unlikely, as hERG can be modulated by ROS generated by various experimental means."
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"The modulation of HERG K + channels by ROS, occurring in both resting and stimulated conditions, may represent an important functional mechanism linking the changes in the levels of O 2 and ROS in hea[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"These results suggested that endogenous iron ions are possibly involved in controlling resting ROS production which, in turn, modulate KCNH2 channel function."
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"In fact, it seems possible to speculate that the increase of the outward currents mediated by HERG caused by the burst of ROS production that follows the reperfusion of the tissue after an ischemic pe[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"These results suggested that histidines in the S 5 -S 6 linker are crucial players in iron dependent ROS production modulating KCNH2 K + channel function."
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"However, excessive production of ROS leads to endothelial dysfunction and changes in molecular pathways that underpin the pathogenesis of CVDs.12 ROS directly or indirectly activate different extracellular stimuli (AngII and TNF-α) as well as induce hypertrophy-linked genes (c-fos, c-jun, and erg-1) which ultimately transform hypertrophic myocytes."
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"We therefore investigated whether ROS, by modulating the interaction of hERG with Hsp90, mediates hypoxia induced hERG downregulation."
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