January 1, 1997Journal of Biological ChemistryOpen Access

The Human ∆1261 Mutation of the HERG Potassium Channel Results in a Truncated Protein That Contains a Subunit Interaction Domain and Decreases the Channel Expression

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Structured PICO

Population

Transfected cells (preclinical model)

Intervention

Expression of truncated HERG proteins containing NAB(HERG), including the delta1261 human mutation

Outcome

Functional expression of the HERG channel and subunit interactionsurrogate

The delta1261 mutation in the HERG potassium channel produces a truncated protein that inhibits functional channel expression, providing a molecular mechanism for the prolonged QT intervals seen in patients with long QT syndrome.

Discussion

No takes yet. Share an insight, caveat, or question.

Implication

Cautions against clinical extrapolation from cell models; leaves open dominant-negative HERG effects in human LQTS.

Cite This Study

Li et al. (1997) studied this question.

synapsesocial.com/papers/6a807b4904b22a52ede48b9b https://doi.org/10.1074/jbc.272.2.705

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The Human ∆1261 Mutation of the HERG Potassium Channel Results in a Truncated Protein That Contains a Subunit Interaction Domain and Decreases the Channel Expression

Structured PICO

Discussion

Implication

Cite This Study

The Human ∆1261 Mutation of the HERG Potassium Channel Results in a Truncated Protein That Contains a Subunit Interaction Domain and Decreases the Channel Expression

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider