Long QT Syndrome-associated Mutations in the Per-Arnt-Sim (PAS) Domain of HERG Potassium Channels Accelerate Channel Deactivation
Author:
Publisher
Elsevier BV
Subject
Cell Biology,Molecular Biology,Biochemistry
Reference38 articles.
1. A molecular basis for cardiac arrhythmia: HERG mutations cause long QT syndrome
2. Missense Mutation in the Pore Region of HERG Causes Familial Long QT Syndrome
3. Four Novel KVLQT1 and Four Novel HERG Mutations in Familial Long-QT Syndrome
4. Novel missense mutation in the cyclic nucleotide-binding domain ofHERG causes long QT syndrome
5. Multiple different missense mutations in the pore region of HERG in patients with long QT syndrome
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1. An intracellular hydrophobic nexus critical for hERG1 channel slow deactivation;Biophysical Journal;2024-01
2. High throughput clone screening on overexpressed hERG1 and Kv1.3 potassium channels using ion channel reader (ICR) label free technology;Heliyon;2023-10
3. Targeted activation of human ether-à-go-go-related gene channels rescues electrical instability induced by the R56Q+/− long QT syndrome variant;Cardiovascular Research;2023-09-21
4. Prediction of Kv11.1 potassium channel PAS-domain variants trafficking via machine learning;Journal of Molecular and Cellular Cardiology;2023-07
5. An intracellular hydrophobic nexus is critical for slow deactivation in hERG channels;2023-03-05
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