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XB-ART-16345
Cell 1997 Jun 27;897:1121-32. doi: 10.1016/s0092-8674(00)80299-8.
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Regulation of IRK3 inward rectifier K+ channel by m1 acetylcholine receptor and intracellular magnesium.

Chuang H , Jan YN , Jan LY .


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Inward rectifier K+ channels control the cell's membrane potential and neuronal excitability. We report that the IRK3 but not the IRK1 inward rectifier K+ channel activity is inhibited by m1 muscarinic acetylcholine receptor. This m1 modulation cannot be accounted for by protein kinase C, Ca2+, or channel phosphorylation, but can be mimicked by Mg2+. Based on quantitative analyses of IRK3 and two different IRK1 mutant channels bestowed with sensitivity to m1 modulation, we suggest that the resting Mg2+ level causes chronic inhibition of IRK3 channels, and m1 receptor stimulation may lead to an increase of cytoplasmic Mg2+ concentration and further channel inhibition, due to the ability of Mg2+ to lead these channels into a prolonged inactivated state.

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Species referenced: Xenopus laevis
Genes referenced: kcnj2 kcnj4