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Cited by 5 publications
(6 citation statements)
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“…But how exactly are arrhythmias triggered under these conditions? Our data show that the cells are confronted with a three-fold challenge: Firstly, K v 7.1- deficient CMs already display a pronounced FPD and action potential prolongation under baseline conditions, as also seen previously in patient-derived hiPSC-CMs (Zhang et al, 2014 ), implying that K v 7.1 does also play a role in the CM ground state (Greber et al, 2015 ). Secondly, adrenergic stimulation induces a chronotropic effect that the cells have to cope with in terms of their repolarization kinetics.…”
Section: Discussionsupporting
confidence: 82%
See 1 more Smart Citation
“…But how exactly are arrhythmias triggered under these conditions? Our data show that the cells are confronted with a three-fold challenge: Firstly, K v 7.1- deficient CMs already display a pronounced FPD and action potential prolongation under baseline conditions, as also seen previously in patient-derived hiPSC-CMs (Zhang et al, 2014 ), implying that K v 7.1 does also play a role in the CM ground state (Greber et al, 2015 ). Secondly, adrenergic stimulation induces a chronotropic effect that the cells have to cope with in terms of their repolarization kinetics.…”
Section: Discussionsupporting
confidence: 82%
“…Although it is beyond doubt that K v 7.1 exerts some basal function in cardiac cells under ground state conditions (Greber et al, 2015 ), we noticed with interest that very little K v 7.1 protein was actually localized to the outer cardiomyocyte membrane (Figure 1D , top panels). Indeed, the concept that K v 7.1 plays a prominent role in unstressed cardiomyocytes, including hiPSC-CMs, is controversial (Christ et al, 2015 ).…”
Section: Resultsmentioning
confidence: 74%
“…This means that depending on the hPSCs selected, the phenotypic variation between lines (up to 400%) can be greater than any change caused by the mutation (usually 10% to 100%). This may explain some of the discrepancies reported in the literature for hPSC-based disease modeling, including for the magnitude of change caused by mutations in KNCQ1 , which underlies long-QT syndrome type 1 [ 33 , 34 ]. Consequently, the use of isogenic pairs is becoming the gold standard for disease modeling using hPSCs.…”
Section: Discussionmentioning
confidence: 99%
“…This may be because binding of RG3 to the serine residue in the pore of I Kr is weak. Also, the impact of RG3 on I Ks activation is likely to be minimal because this current is relatively small and there has been controversy over whether it makes a meaningful contribution to repolarization in hiPSC-CMs [ 53 , 54 ]. For NS1643, we observed potent responses at all concentrations tested, which was surprising.…”
Section: Discussionmentioning
confidence: 99%