IndraLab

Statements

PPP3 dephosphorylates KCNB1. 16 / 17
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"Variable calcineurin-dependent dephosphorylation of Kv2.1 at 16 phosphorylated residues generates an activity gradient for channel gating and neuronal firing."
21730325
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"It has been proposed that inhibition of N-type Ca channels, known to be located at C-bouton synapses (Wilson et al., 2004), by G -dependent pathways following M2 receptor activation could lower the levels of local intracellular Ca , thus reducing calcineurin-related dephosphorylation of Kv2.1 channels (Deardorff et al., 2014; Romer et al., 2019)."
32081133
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"Upon increased neuronal activity, calcineurin directly or indirectly induces persistent dephosphorylation of Kv2.1 and leads to dispersion of Kv2.1 clusters."
15950285
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"Our study demonstrates that SDF-1α acts upon neuronal CXCR4 to induce an NMDA receptor-dependent elevation in [Ca 2+ ] i , leading to calcineurin-dependent dephosphorylation of Kv2.1, dispersal of channel clusters and enhancement of voltage-dependent activation of Kv2.1/ I DR currents."
23223293
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"Upon increased neuronal activity, calcineurin directly or indirectly induces persistent dephosphorylation of Kv2.1 and leads to dispersion of Kv2.1 clusters."
15950285
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"One SNP (rs756529) is intragenic within KCNB1 , which is dephosphorylated by calcineurin, a previously reported candidate gene for LV hypertrophy within this population [ xref ]."
19454037
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"In that respect, previous studies have shown that activity- and calcineurin-dependent Kv2.1 dephosphorylation induces hyperpolarizing shifts."
26890139
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"This shift was blocked by WZ811 (100 nM), MK-801 (10 μM), and the calcineurin inhibitor FK506 (10 μM; xref ), suggesting that SDF-1α/CXCR4-induced elevations in [Ca 2+ ] i result in calcineurin-dependent dephosphorylation of the Kv2.1 channel protein."
23223293
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"We previously found that reversible calcineurin-dependent Kv2.1 dephosphorylation as induced by ischemic insult is neuroprotective. xref However, sustained activation of Kv2.1, as occurs upon induction of apoptosis xref , or prolonged treatment with high levels of glutamate xref , might lead to excessive K + efflux, and subsequent induction of apoptotic or excitotoxic cell death, as we suggested previously. xref "
19276663
sparser
"One SNP (rs756529) is intragenic within KCNB1 , which is dephosphorylated by calcineurin, a previously reported candidate gene for LV hypertrophy within this population."
19454037
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"During ischemia, increased intracellular zinc concentrations also induce calcineurin-dependent dephosphorylation of Kv2.1, which causes dispersal of channel clusters on the plasma membrane."
20606213
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"Activity-dependent Kv2.1 dephosphorylation by calcineurin induces graded hyperpolarizing shifts in voltage-dependent activation, causing suppression of neuronal excitability."
16917065
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"For example, cytosolic Ca 2+ increase and subsequent calcineurin activation affects the gating kinetics of I DR channels via dephosphorylating Kv2.1 channels, since calcineurin-dependent dephosphorylation of Kv2.1 decreases the threshold for I DR channel opening and disrupts channel clustering, resulting in changes of activation kinetics [ xref xref ]."
28280420
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"However, long-term elevation of intracellular [Ca 2+ ] can result in calcineurin-dependent dephosphorylation of Kv2.1, impacting its voltage activation properties and eliminating its clustering at ER–PM junctions [ xref , xref ]."
35216068
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"In addition, activity-dependent Kv2.1 dephosphorylation by CaN induces a hyperpolarizing shift in the voltage-dependent activation of channels, causing a decrease in neuronal excitability ( xref )."
21273417
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"We previously found that seizures in rats in vivo , or glutamate stimulation of cultured rat hippocampal pyramidal neurons, led to calcineurin-dependent dephosphorylation of Kv2.1, and dispersion of Kv2.1 clusters. xref Initial experiments showed that glutamate stimulation of cultured neurons also led to significant hyperpolarizing shifts in voltage-dependent activation of neuronal I K . xref However, the potential impact of these changes on neuronal function could not be accurately deduced without a more comprehensive analysis of the effects of glutamate stimulation on the gating properties of neuronal Kv2.1 channels."
19276663