Key result
Mutant Rad overexpression prolongs QT intervals and induces diverse arrhythmias in mice.
Why the study?
The role of Rad, a small GTP-binding protein highly expressed in the heart, in regulating L-type Ca2+ channels and cardiac arrhythmias was unknown.
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Rad modulation of cardiac calcium currents may influence excitability; leaves open therapeutic targeting in human arrhythmias.
Yada et al. (2007) studied Arrhythmias and QT prolongation. Overexpression of dominant negative mutant Rad (S105N) vs. Wild-type littermate mice was evaluated on Action potential duration, QT prolongation, and diverse arrhythmias. Overexpression of dominant negative mutant Rad (S105N) in transgenic mice caused significant action potential and QT prolongation and induced diverse arrhythmias compared to wild-type mice.
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