Associated Papers
Nutritional Factors and Arrhythmic Risk in Long QT Syndrome: A Narrative Review of Mechanistic and Clinical Evidence.
Mazzanti A et al.
Advances in Nutrition (bethesda, Md.), 2025
Rescue of expression and function of long QT syndrome-causing mutant hERG channels by enhancing channel stability in the plasma membrane.
Davis J et al.
The Journal of Biological Chemistry, 2024
Differential Effects of Remdesivir and Lumacaftor on Homomeric and Heteromeric hERG Channels.
Campagna N et al.
Molecular Pharmacology, 2023
Glycosylation stabilizes hERG channels on the plasma membrane by decreasing proteolytic susceptibility.
Lamothe SM et al.
Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology, 2018
The role of monoubiquitination in endocytic degradation of human ether-a-go-go-related gene (hERG) channels under low K+ conditions.
Sun T et al.
The Journal of Biological Chemistry, 2011
Involvement of caveolin in low K+-induced endocytic degradation of cell-surface human ether-a-go-go-related gene (hERG) channels.
Massaeli H et al.
The Journal of Biological Chemistry, 2010
Extracellular K+ is a prerequisite for the function and plasma membrane stability of HERG channels.
Massaeli H et al.
Circulation Research, 2010
The 5-HT2 antagonist ketanserin is an open channel blocker of human cardiac ether-à-go-go-related gene (hERG) potassium channels.
Tang Q et al.
British Journal of Pharmacology, 2008
Functional interaction between extracellular sodium, potassium and inactivation gating in HERG channels.
Mullins FM et al.
The Journal of Physiology, 2004
Extracellular sodium interacts with the HERG channel at an outer pore site.
Mullins FM et al.
The Journal of General Physiology, 2002
Mutational analysis of block and facilitation of HERG current by a class III anti-arrhythmic agent, nifekalant.
Hosaka Y et al.
Channels (austin, Tex.), 0
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