IndraLab

Statements


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"Inhaled anesthetics xenon , diethyl ether , halothane , and chloroform robustly activate TREK-1 at concentrations relevant to their clinical use ( 30 , 31 ) ."

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"Halothane activation of the related K2P channels TREK1 and TASK1 could be abolished by mutating a 6 amino acid motif located in the C-terminal domain (Talley and Bayliss, 2002), suggesting that haloth[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Chloroform, diethyl ether, halothane and isoflurane activated TREK-1, whereas only halothane and isoflurane activated TASK."

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"Chloroform, diethyl ether, halothane and isoflurane activate TREK-1, whereas only halothane and isoflurane activate TASK."

No evidence text available

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"As previously reported, arachidonic acid (20 microM) stimulated all of these channels, and a volatile anesthetic, halothane (1 mM) augmented TREK-1 and TREK-2 but not TRAAK."

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"XREF_BIBR examined TASK and TREK-1, and found that TREK-1 was activated by chloroform, diethyl ether, halothane and isoflurane, while TASK was activated by halothane and isoflurane."

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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."