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Calcium(2+) activates KCNK18. 24 / 29
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"TRESK is activated by the elevation of cytoplasmic calcium concentration via calcineurin in HEK293 cells."
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"Combined extracellular application of calcium (2 mM) and the calcium-ionophore ionomycin (1 microM) activated TRESK current by 50 +/-12% (n = 6, gray control curves, XREF_FIG, for further comments on this stimulation see XREF_SUPPLEMENTARY)."
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"51 TRESK currents are strongly potentiated by increases in intracellular Ca 2+ mediated by calcineurin through an NFAT-like binding site (Pro-Gln-Iso-Asn-Iso-Val) within the TM2-TM3 intracellular loop[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"TRESK is activated in a complex manner by intracellular calcium signalling."
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"These data indicate that TRESK is activated by increased cytoplasmic calcium concentration."
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"The K356A and R361A mutations diminished the calcium-dependent activation of TRESK, evoked by the calcium-ionophore ionomycin, as determined by conventional TEVC measurements (Fig. 5, A and B)."
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"TRESK is activated by calcium involving the calcium/calmodulin-dependent protein phosphatases in cell models and has been suggested being the target of the Sichuan pepper ingredient sanshool in sensory neurons [64]."
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"Intracellular Ca 2+ -induced activation of the TRESK channel is regulated by interaction with calcineurin and 14-3-3eta [XREF_BIBR XREF_BIBR]."
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"14-3-3 proteins also alter the kinetics of calcium-dependent enhanced activity of the TWIK-related spinal cord K+ channel (TRESK) by directly binding to the intracellular loop of TRESK [14]."
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"Thus, it could support a more robust and sustained Ca 2+ signal, via a positive feedback loop as TRESK and CRAC may support each other 's activity mutually : TRESK activation by Ca 2+ - Cn and CRAC activation by TRESK mediated hyperpolarization."
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"We did not explore further the change in the calcium pattern, but it is tempting to speculate that the TRESK activation by Ca /calcineurin might limit depolarization and Ca influx, thus preventing excessive neuronal activation."
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"An increase in the Ca influx by ionomycin, an effective Ca ionophore, activates the TRESK channel [4]."
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"Among the K2P type potassium channel family, only TRESK channels are activated by elevations in the cytoplasmic Ca 2+ concentration via dephosphorylation by calcineurin (protein phosphatase 2B [PP2B])[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"If the TRESK channel is affected by extracellular Ca levels, a blockade of the Ca influx through Ca channels will inhibit the activity of the TRESK channel."
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"However, TRESK channel is blocked by Ca channel blockers."
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"The unique calcium dependent activation of TRESK relies on the long cytoplasmic loop of the channel, a distinguishing structural element in the K2P family XREF_BIBR."
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"Elevation of the cytoplasmic Ca 2+ concentration activates TRESK."
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"Among Ca 2+ -associated K2P channels, TRESK is unique because TRESK channels are activated by elevations in the cytoplasmic Ca 2+ concentration via dephosphorylation by calcineurin, whereas other Ca 2[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"We reasoned that glutamate induced Ca 2+ entry and depolarisation should activate TRESK, since uniquely TRESK is the only K2P with a calcium sensing domain."
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"Since calcium mediated calcineurin activation has previously been shown to activate TRESK 5, we propose that TRESK is an essential component of the negative feedback regulation of glutamate receptor associated calcium influx."
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"Cloxyquin activates TRESK in its resting state, by a mechanism independent of Ca /calcineurin-mediated dephosphorilation."
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"We first assumed that Ca channel blockers could inhibit TRESK activity, because it is known that the TRESK channel is activated by an increase in [Ca ] [1,2]."
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"Ca /CN activates TRESK, which contains a PxIxIT and an LxVP motif that mediate dephosphorylation of the channel [67, 68]."
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"In contrast to other K 2P channels expressed in sensory neurons, TRESK is activated by intracellular calcium increases through calcineurin, thus acting as a " brake " to prevent excessive activation of sensory neurons in response to depolarizing stimuli."
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