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Comment
. 2015 Apr 21;112(16):E1969.
doi: 10.1073/pnas.1503762112. Epub 2015 Mar 20.

Reply to Christ et al.: LQT1 and JLNS phenotypes in hiPSC-derived cardiomyocytes are due to KCNQ1 mutations

Boris Greber  1 , Arie O Verkerk  2 , Guiscard Seebohm  3 , Christine L Mummery  4 , Milena Bellin  5
Affiliations
Comment

Reply to Christ et al.: LQT1 and JLNS phenotypes in hiPSC-derived cardiomyocytes are due to KCNQ1 mutations

Boris Greber et al. Proc Natl Acad Sci U S A. .
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

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References

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    1. Christ T, Horvath A, Eschenhagen T. LQT1-phenotypes in hiPSC: Are we measuring the right thing? Proc Natl Acad Sci USA. 2015;112:E1968. - PMC - PubMed
    1. Towart R, et al. Blockade of the I(Ks) potassium channel: An overlooked cardiovascular liability in drug safety screening? J Pharmacol Toxicol Methods. 2009;60(1):1–10. - PubMed
    1. Moretti A, et al. Patient-specific induced pluripotent stem-cell models for long-QT syndrome. N Engl J Med. 2010;363(15):1397–1409. - PubMed
    1. Wang K, et al. Biophysical properties of slow potassium channels in human embryonic stem cell derived cardiomyocytes implicate subunit stoichiometry. J Physiol. 2011;589(Pt 24):6093–6104. - PMC - PubMed

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