Key result
Fluorescence lifetime measurements of KcsA channels demonstrate that the opening of the bundle crossing is insufficient for ion conduction, revealing the existence of a second gate in the permeation pathway.
Population
KcsA channels (wild-type and mutants A73E and E71A) labeled with tetramethylrhodamine
Comparison
Mutations A73E and E71A vs Wild-type KcsA channel
Design
Preclinical
Authors
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Questions sufficiency of bundle crossing for K+ conduction in cardiac models; leaves open selectivity filter gating as arrhythmia mechanism.
Fluorescence lifetime spectroscopy reveals the existence of a second gate, likely the selectivity filter, for ion conduction in KcsA channels.
Blunck et al. (2006) studied KcsA potassium channel gating. pH-dependent gating and mutations (A73E, E71A) vs. Wild-type KcsA was evaluated on Fluorescence lifetime and open probability. Fluorescence lifetime measurements of KcsA channels demonstrate that the opening of the bundle crossing is insufficient for ion conduction, revealing the existence of a second gate in the permeation pathway.
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