title: Reply to Christ et al.: LQT1 and JLNS phenotypes in hiPSC-derived cardiomyocytes are due to KCNQ1 mutations.
authors: Human Stem Cell Pluripotency Laboratory, Max Planck Institute for Molecular Biomedicine, D-48149 Münster, Germany; Chemical Genomics Centre of the Max Planck Society, 44227 Dortmund, Germany; boris.greber@mpi-muenster.mpg.de m.bellin@lumc.nl.
authors: Boris
authors: B
authors: Greber
authors: Department of Anatomy, Embryology, and Physiology, Heart Failure Research Center, Academic Medical Center, Amsterdam 1105 AZ, The Netherlands;
authors: Arie O
authors: AO
authors: Verkerk
authors: Department of Cardiovascular Medicine, Institute for Genetics of Heart Diseases, University Hospital Münster, D-48149 Münster, Germany; and.
authors: Guiscard
authors: G
authors: Seebohm
authors: Department of Anatomy and Embryology, Leiden University Medical Center, Leiden 2300 RC, The Netherlands.
authors: Christine L
authors: CL
authors: Mummery
authors: Department of Anatomy and Embryology, Leiden University Medical Center, Leiden 2300 RC, The Netherlands boris.greber@mpi-muenster.mpg.de m.bellin@lumc.nl.
authors: Milena
authors: M
authors: Bellin
mesh_terms: D006801:Humans; D057026:Induced Pluripotent Stem Cells / Q000502:physiology*; D029593:Jervell-Lange Nielsen Syndrome / Q000188:drug therapy* / Q000235:genetics* / Q000503:physiopathology*; D051657:KCNQ1 Potassium Channel / Q000235:genetics*; D008954:Models, Biological; D010641:Phenotype
chemical_list: D051657:KCNQ1 Potassium Channel