Correction of Defective Protein Trafficking of a Mutant HERG Potassium Channel in Human Long QT Syndrome
Author:
Publisher
Elsevier BV
Subject
Cell Biology,Molecular Biology,Biochemistry
Reference29 articles.
1. A molecular basis for cardiac arrhythmia: HERG mutations cause long QT syndrome
2. SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome
3. Positional cloning of a novel potassium channel gene: KVLQT1 mutations cause cardiac arrhythmias
4. Mutations in the hminK gene cause long QT syndrome and suppress lKs function
5. MiRP1 Forms IKr Potassium Channels with HERG and Is Associated with Cardiac Arrhythmia
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1. Rescue of expression and function of long QT syndrome-causing mutant hERG channels by enhancing channel stability in the plasma membrane;Journal of Biological Chemistry;2024-08
2. The proteostasis interactomes of trafficking-deficient variants of the voltage-gated potassium channel KV11.1 associated with long QT syndrome;Journal of Biological Chemistry;2024-07
3. Ligand-based virtual-screening identified a novel CFTR ligand which improves the defective cell surface expression of misfolded ABC transporters;Frontiers in Pharmacology;2024-04-11
4. PIEZO1 and PIEZO2 Blade domains are differentially required for channel localization and function;2024-04-10
5. Functional and clinical characterization of a novel homozygous KCNH2 missense variant in the pore region of Kv11.1 leading to a viable but severe long-QT syndrome;Gene;2024-03
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