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Statements

PPP3 activates KCNK18. 12 / 15
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"Calcineurin Modulation of TRESK and Pain Sensitivity."
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"It has been shown that an increase of intracellular calcium produced by the calcium ionophore ionomycin, can produce calcineurin-dependent activation of TRESK expressed in Xenopus oocytes xref ."
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"Using a model of pain hypersensitivity in bone cancer–bearing rats, the authors show that intrathecal injection of calcineurin enhances TRESK mRNA and protein expression, as well as TRESK-mediated current [41]."
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"This data indicates that calcineurin inhibition deactivates TRESK channels through the suppression of TRESK dephosphorylation but also reduces TRESK protein and mRNA abundance."
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"Intriguingly, dysarthria, restlessness, headache and seizures have been observed in our patients and it is tempting to speculate that these symptoms could be associated, at least in part, with Y163D- and S252L-induced disruption of calcineurin-dependent TRESK channel activation in the brain."
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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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"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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"TRESK expressed in Xenopus oocytes is strikingly activated by calcineurin in response to calcium mobilizing stimulation xref , xref , and it is assumed that native TRESK in neuronal cells is subject to similar regulation ( xref )."
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"Because inhibiting calcineurin will impair TRESK activation in response to stimuli-induced Ca increase, a higher requirement of this volatile anesthetic will be needed to achieve anesthesia, as recently shown in the knockout mice [61]."
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"Intrathecal application of exogenous calcineurin to tumor-bearing rats rescued TRESK abundance and abrogated both DRG hyperexcitability and pain hypersensitivity, whereas either inhibition or knockdown of calcineurin in normal rats reduced TRESK abundance and increased DRG excitability and pain sensitivity."
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"TRESK channel is inhibited by arachidonic acid [59] but directly activated by calcineurin after G q receptor stimulation and a subsequent rise in intracellular calcium [89]."
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"When the T-cell is activated, binding and dephosphorylation of calcineurin to the NFAT-docking site of TRESK could induce activation of NFAT and TRESK."
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