Related Experiment Video
Updated: May 3, 2026

Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b
Published on: November 11, 2016
Allitridin reduces I Kr current by disrupting the trafficking of human ether-à-go-go-related gene channels
Guoliang Li1, Gong Cheng, Jine Wu
1Department of Cardiovascular Medicine, First Affiliated Hospital of Xi'an Jiaotong University College of Medicine, Institute of Cardiovascular Channelopathy, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, and Key Laboratory of Molecular Cardiology, Xi'an, PR China.
Objectives:
To investigate the effects of allitridin on human ether-à-go-go-related gene (hERG) channels.
Methods:
We used whole-cell patch clamping and laser confocal scanning microscopy to evaluate the effects of allitridin on hERG currents and the membrane expression of the hERG protein expressed in HEK 293 cells.
Results:
The amplitude of IKr showed a concentration-dependent decrease with increasing allitridin concentration. Additionally, alterations in the gating properties of hERG channels were also confirmed. Allitridin does not alter the voltage- and time-dependent activation of hERG channels, the gating properties of hERG channel inactivation over time or the recovery from inactivation, but allitridin does cause alterations in the steady-state inactivation and the deactivation of hERG channels. We further evaluated the influence of allitridin on membrane expression of the hERG protein. Images of allitridin-treated cells showed a reduction in hERG protein on the membrane and retention in the cytoplasm.
Conclusions:
To the best of our knowledge this is the first study to show that allitridin reduces the IKr current by impairing the trafficking of hERG channels. The results may demonstrate that allitridin could be a promising candidate for the prevention and treatment of arrhythmia-related diseases.
More Related Videos
10:07High-throughput Screening for Small-molecule Modulators of Inward Rectifier Potassium Channels
Published on: January 27, 2013
08:03Hybrid Cell Analysis System to Assess Structural and Contractile Changes of Human iPSC-Derived Cardiomyocytes for Preclinical Cardiac Risk Evaluation
Published on: October 20, 2022
Related Concept Videos
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
Drugs Affecting Neurotransmitter Release or Uptake
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...