November 1, 2003Journal of Biological ChemistryOpen Access

Modulation of Cardiac Sodium Channel Gating by Protein Kinase A Can Be Altered by Disease-linked Mutation

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Population

Wild type and three disease-linked C-terminal mutant cardiac sodium channels associated with Long-QT syndrome

Comparison

Protein kinase A (PKA) stimulation vs Wild type channels and unstimulated state

Design

Preclinical

Authors

MTMichihiro TateyamaNational Institute for Physiological Sciences IRIlaria RivoltaUniversità Cattolica del Sacro Cuore CCColleen E. ClancyElectrophysiology

Discussion

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Implication

Highlights mutation-specific PKA effects in LQTS models; hypothesis-generating and should not yet alter clinical practice.

Structured PICO

Population

Wild type and three disease-linked C-terminal mutant cardiac sodium channels (D1790G, Y1795C, and Y1795H) associated with Long-QT syndrome

Intervention

Protein kinase A (PKA) stimulation

Comparator

Wild type channels and unstimulated state

Outcome

Sustained macroscopic current and channel gating (bursting)surrogate

The charge at position 1790 of the C terminus modulates the response of the cardiac sodium channel to PKA stimulation, providing mechanistic insight into Long-QT syndrome mutations.

Cite This Study

Tateyama et al. (2003) studied this question.

synapsesocial.com/papers/6a6f7efbfe4101aa97dfcd94 https://doi.org/10.1074/jbc.m308977200

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Modulation of Cardiac Sodium Channel Gating by Protein Kinase A Can Be Altered by Disease-linked Mutation

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Modulation of Cardiac Sodium Channel Gating by Protein Kinase A Can Be Altered by Disease-linked Mutation

Discussion

Member takes

Implication

Structured PICO

Cite This Study

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