Abstract:
:The idiopathic short QT syndrome (SQTS) is characterised by an abnormally short QT interval on the electrocardiogram and by an increased risk of arrhythmia and sudden death. One variant of the syndrome is linked to missense mutations that lead to a single amino-acid change (N588K; asparagine to lysine) in the S5-Pore linker region of the cardiac HERG K(+) channel. This study was performed in order to determine how the N588K mutation alters HERG channel current (I(HERG)) kinetics at mammalian physiological temperature. The whole-cell current-voltage (I-V) relation for wild-type (WT) I(HERG) measured from Chinese Hamster Ovary cells was maximal at approximately 0 mV and showed marked inward rectification positive to this. In contrast, N588K I(HERG) showed marked rectification only at +60 mV and at more positive voltages. The voltage dependence of activation of N588K-HERG did not differ significantly from that of WT-HERG. However, N588K I(HERG) had a significantly more positive inactivation V(0.5) (-8.14+/-0.82 mV) than did WT I(HERG) (-70.05+/-0.82 mV; P<0.001, unpaired t test; n=5 for each). Its P(Na)/P(K) ratio was also greater. The instantaneous I-V relation for N588K I(HERG) under action potential voltage clamp peaked at approximately +40 mV, compared to approximately -37 mV for WT-I(HERG). These findings underscore the importance of the S5-P linker in HERG channel function and indicate that N588K-HERG contributes increased repolarising current earlier in the ventricular action potential at physiological temperature due to a approximately +60 mV shift in voltage dependence of I(HERG) inactivation.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
McPate MJ,Duncan RS,Milnes JT,Witchel HJ,Hancox JCdoi
10.1016/j.bbrc.2005.06.112subject
Has Abstractpub_date
2005-08-26 00:00:00pages
441-9issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(05)01331-8journal_volume
334pub_type
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