IndraLab

Statements

Xenon(0) activates KCNK2. 7 / 7
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"TREK-1 is markedly activated by clinically relevant concentrations of nitrous oxide, xenon, and cyclopropane."
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"The two-pore domain potassium channel TREK-1 is activated by xenon [XREF_BIBR]."
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"There is some variation in response: the anesthetic gas N O activates TREK-1 and TRESK but not TASK-3 ; similarly, xenon and cyclopropane activate TREK-1 but not TASK-3 ; chloroform inhibits TASK-1, and halothane inhibits THIK-1 (Supplemental Digital Content, Online Supplement S2, http://links.lww.com/AA/F214, summarizes work in this area)."
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"Although the dose–response curves for xenon suggested it bound to the channel relatively weakly, xenon markedly activated TREK-1 over a clinically relevant range of concentrations."
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"Recently, TREK-1 gene was found to be activated by xenon, which is considered to be associated with the activation of Ca channels, reduction of glutamate release and inhibition of excitotoxicity (Zhao et al., 2018)."
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"For example, xenon can activate K channels (TREK-1), thereby causing hyperpolarization of the membrane potential and a reduction in the activation threshold [96]."
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"XREF_BIBR expressed TREK-1 channels on HEK-293 cells and showed that TREK-1 currents were enhanced by nitrous oxide, xenon, cyclopropane and halothane."
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