Population
Xenopus oocytes or HEK293T cells expressing cloned inward rectifier K+ channel Kir2.1 (IRK1) mutants
Comparison
Single-point mutations and double-point mutation… vs Wild-type (WT) Kir2.1
Design
Preclinical
Authors
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Glu299/Glu224 sites modulate Kir2.1 rectification in animal models; leaves open human arrhythmia relevance without further validation.
Glu299 and Glu224 are critical sites controlling rectification and permeation in the Kir2.1 K+ channel, likely facilitating spermine entry and exit at the blocking site.
Kubo et al. (2001) studied this question.
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