High-throughput discovery of trafficking-deficient variants in the cardiac potassium channel K<sub>V</sub>11.1.

导出 OA

翻译打印收藏纠错

第一作者： Krystian A,Kozek

第一单位： Vanderbilt Center for Arrhythmia Research and Therapeutics, Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

作者： Krystian A,Kozek ^[1] ; Andrew M,Glazer ^[1] ; Chai-Ann,Ng ^[2] ; Daniel,Blackwell ^[1] ; Christian L,Egly ^[1] ; Loren R,Vanags ^[1] ; Marcia,Blair ^[1] ; Devyn,Mitchell ^[1] ; Kenneth A,Matreyek ^[3] ; Douglas M,Fowler ^[4] ; Bjorn C,Knollmann ^[1] ; Jamie I,Vandenberg ^[2] ; Dan M,Roden ^[1] ; Brett M,Kroncke ^[5]

作者单位： Vanderbilt Center for Arrhythmia Research and Therapeutics, Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee. ^[1] Molecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Darlinghurst, New South Wales, Australia; St Vincent's Clinical School, UNSW Sydney, Darlinghurst, New South Wales, Australia. ^[2] Department of Genome Sciences, University of Washington, Seattle, Washington. ^[3] Department of Genome Sciences, University of Washington, Seattle, Washington; Department of Bioengineering, University of Washington, Seattle, Washington. ^[4] Vanderbilt Center for Arrhythmia Research and Therapeutics, Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address: brett.m.kroncke.1@vumc.org. ^[5]

关键词 Deep mutational scanning K(V)11.1 KCNH2 Membrane trafficking hERG