Key result
Mutating the intrinsic ligand residues Y699 and L701 in the CNBhD of human EAG1 channels impairs channel function by slowing activation and shifting the conductance-voltage relation.
Population
Human EAG1 (KCNH) channels
Comparison
Mutation of intrinsic ligand residues Y699 and… vs Wild-type human EAG1 channels
Design
Preclinical
Authors
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Supports CNBhD ligand role in KCNH gating; leaves open relevance to human cardiac excitability or channelopathies.
The intrinsic ligand within the CNBhD of KCNH channels is essential for promoting voltage sensor activation and stabilizing the open pore.
Zhao et al. (2017) studied this question. Mutation of Y699 and L701 in the CNBhD vs. Wild-type channels was evaluated on Channel activation and conductance-voltage (G-V) relation. Mutating the intrinsic ligand residues Y699 and L701 in the CNBhD of human EAG1 channels impairs channel function by slowing activation and shifting the conductance-voltage relation.
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