August 1, 1996The Journal of General PhysiologyOpen Access

Role of an S4-S5 linker in sodium channel inactivation probed by mutagenesis and a peptide blocker.

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Population

Human heart Na channels (hH1)

Comparison

Mutagenesis of conserved methionine residues on… vs Wild-type hH1 channels

Design

Preclinical

Authors

LTLin TangBGI Group (China)RKRoland G. KallenElectrophysiology RHR HornZoological Society of San Diego

Discussion

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Implication

Findings in animal Na channels leave open relevance to human arrhythmias; hypothesis-generating for S4-S5 linker-targeted modulators.

Structured PICO

Population

Human heart Na channels (hH1)

Intervention

Mutagenesis of conserved methionine residues on the cytoplasmic linker between segments S4 and S5 (M1651M1652/QQ or MM/AA) and cytoplasmic application of pentapeptide KIFMK

Comparator

Wild-type hH1 channels

Outcome

Inactivation kinetics and voltage dependence of inactivationsurrogate

The conserved methionine residues on the S4-S5 linker of human heart Na channels are critical for inactivation kinetics, and peptide block by KIFMK requires open channels and does not mimic the natural inactivation process.

Cite This Study

Tang et al. (1996) studied this question.

synapsesocial.com/papers/6a71a080ce524a4339c510d8 https://doi.org/10.1085/jgp.108.2.89

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Bookmark

Role of an S4-S5 linker in sodium channel inactivation probed by mutagenesis and a peptide blocker.

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Role of an S4-S5 linker in sodium channel inactivation probed by mutagenesis and a peptide blocker.

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider