December 1, 2002Journal of Biological ChemistryOpen Access

A Novel Mutation (T65P) in the PAS Domain of the Human Potassium Channel HERG Results in the Long QT Syndrome by Trafficking Deficiency

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Population

In vitro cell model expressing the novel missense mutation T65P in the PAS domain of the human potassium…

Comparison

Decreased cell incubation temperature and… vs Wild-type HERG channels and standard incubation…

Design

Preclinical

Authors

APAimée PaulussenMaastricht University Medical Centre ARAdam RaesKU Leuven GMGert MatthijsVIB-KU Leuven Center for Cancer Biology

Discussion

Member takes

Implication

Trafficking rescue of T65P HERG remains experimental; leaves open clinical applicability in LQT2.

Structured PICO

Population

In vitro cell model expressing the novel missense mutation T65P in the PAS domain of the human potassium channel HERG

Intervention

Decreased cell incubation temperature (27 degrees C) and pharmacological agents (cisapride and E-4031)

Comparator

Wild-type HERG channels and standard incubation temperature (37 degrees C)

Outcome

Protein trafficking to the cell membrane and channel kineticssurrogate

Identifies a novel HERG mutation (T65P) causing long QT syndrome via trafficking deficiency, which can be rescued by temperature reduction or specific pharmacological agents.

Cite This Study

Paulussen et al. (2002) studied this question.

synapsesocial.com/papers/6a0f9dcad03631df9ce9ccdb https://doi.org/10.1074/jbc.m206569200

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A Novel Mutation (T65P) in the PAS Domain of the Human Potassium Channel HERG Results in the Long QT Syndrome by Trafficking Deficiency

Discussion

Member takes

Implication

Structured PICO

Cite This Study

A Novel Mutation (T65P) in the PAS Domain of the Human Potassium Channel HERG Results in the Long QT Syndrome by Trafficking Deficiency

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider