IndraLab

Statements


AMPK inhibits KCNK2. 6 / 6
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"The effects of azide on TREK occlude subsequent channel inhibition by AMPK and are attenuated by expression of a dominant negative catalytic subunit of AMPK (dnAMPK), suggesting that metabolic stress modulates TREK channels by an AMPK mechanism."

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"XREF_BIBR Instead, they found that AMPK activation inhibited the activity of the two related channels TREK-1 and TREK-2."

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"To the extent that carotid body O (2) sensitivity is dependent on AMPK, our finding that TREK-1 and TREK-2 channels are inhibited by AMPK suggests that TREK channels may represent the AMPK inhibited background K (+) channels that mediate activation of glomus cells by hypoxia."

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"We found that TREK-1 and TREK-2 channels but not TASK-1 or TASK-3 channels are inhibited by AMPK."

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"For studies in HEK 293 cells, TREK-1 and TREK-2 channels as K2P channels could be inhibited by AMPK but not KCNK3 or TASK-3 channels [43], which is not consistent with our study."

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"However, AMPK is known to contribute to hyperpolarizing shifts in the voltage dependence of Nav1.5, decreased amplitudes of BK , TASK, and TREK channel currents, and decreased membrane expression of Kv7.1 and Kir2.1 channels [5],all effects that would presumably enhance cellular activity."