Key result
Intracellular acidification strongly inhibits Kir2.3 channels through proton-mediated interactions between the N- and C-terminal domains involving C-terminal histidine residues.
Population
In vitro models of Kir2.3 (HIR) inward rectifier K+ channels
Comparison
Intracellular acidification vs Normal physiological pH (pH 7.4)
Design
Preclinical
Authors
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May modulate cardiac excitability in acidosis; leaves open validation in human disease models.
Demonstrates a novel mechanism for K+ channel gating where intracellular protons mediate the interaction between N- and C-terminal domains to close the channel.
Qu et al. (2000) studied this question. Intracellular acidification / protons vs. Physiological pH (7.4) was evaluated on Channel gating and N/C-terminal interaction. Intracellular acidification strongly inhibits Kir2.3 channels through proton-mediated interactions between the N- and C-terminal domains involving C-terminal histidine residues.
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