scholarly journals MinkS38G Gene Polymorphism and Atrial Fibrillation in the Chinese Population: A Meta-Analysis of 1871 Participants

2014 ◽  
Vol 2014 ◽  
pp. 1-6
Author(s):  
Yan-yan Li ◽  
Lian-sheng Wang ◽  
Xin-zheng Lu
Keyword(s):  
Atrial Fibrillation ◽  
Gene Polymorphism ◽  
Potassium Channel ◽  
Chinese Population ◽  
Meta Analysis ◽  
Delayed Rectifier ◽  
Channel Current ◽  
Delayed Rectifier Potassium Channel ◽  
The Individual ◽  
Rectifier Potassium Channel

Minkgene S38G polymorphism in theβ-subunit of slow activating component of the delayed rectifier potassium channel current potassium channel has been associated with increased atrial fibrillation (AF) risk. However, the individual studies results were still controversial. To investigate the association ofMinkS38G gene polymorphisms with AF, a meta-analysis including 1871 subjects from six individual studies was conducted.MinkS38G gene polymorphism was significantly related to AF under allelic (OR: 1.380, 95% CI: 1.200–1.600,P<0.00001), recessive (OR: 1.193, 95% CI: 1.033–1.377,P=0.017), dominant (OR: 1.057, 95% CI: 1.025–1.089,P<0.00001), additive (OR: 1.105, 95% CI: 1.036–1.178,P=0.002), homozygous (OR: 1.128, 95% CI: 1.068–1.191,P<0.00001), and heterozygous genetic models (OR: 1.078, 95% CI: 1.014–1.146,P=0.016). A significant association betweenMinkS38G gene polymorphism and AF risk was found. G allele carriers may predispose to AF.

Cardiomyocyte slowly activating delayed rectifier potassium channel: regulation by exercise and β-adrenergic signaling

2020 ◽  
Vol 128 (5) ◽  
pp. 1177-1185 ◽  
Author(s):  
Xinrui Wang ◽  
Robert H. Fitts
Keyword(s):  
Exercise Training ◽  
Action Potential ◽  
Potassium Channel ◽  
Delayed Rectifier ◽  
Adrenergic Signaling ◽  
Channel Current ◽  
Channel Regulation ◽  
Anchoring Protein ◽  
Delayed Rectifier Potassium Channel ◽  
Rectifier Potassium Channel

Results demonstrate that exercise training (TRN) downregulates ventricular IKs channel current and the channel’s responsiveness to β-agonist factors mediated by TRN-induced decline in channel subunits KCNQ1 and KCNE1 and the A-kinase anchoring protein yotiao. The reduced IKs current helps explain the TRN-induced prolongation of the action potential in basal conditions and, coupled with previously reported upregulation of the KATP channel, results in a more efficient heart that is better able to respond to beat-by-beat changes in metabolism.

scholarly journals Effects of Injectable HPβCD-Diclofenac on the Human Delayed Rectifier Potassium Channel Current In Vitro and on Proarrhythmic QTc In Vivo

2013 ◽  
Vol 35 (5) ◽  
pp. 646-658 ◽  
Author(s):  
Daniel B. Carr ◽  
Tara McDonnell Moorehead ◽  
Annie Bouchard ◽  
Craig R. Sprenger ◽  
Douglas A. Hamilton ◽  
...  
Keyword(s):  
Potassium Channel ◽  
Delayed Rectifier ◽  
Channel Current ◽  
Delayed Rectifier Potassium Channel ◽  
Rectifier Potassium Channel

scholarly journals Electrophysiological Evaluation of an Anticancer Drug Gemcitabine on Cardiotoxicity Revealing Down-regulation and Modification of the Activation Gating Properties in the Human Rapid Delayed Rectifier Potassium Channel

2021 ◽  
Author(s):  
Mengyan Wei ◽  
Pu Wang ◽  
Xiufang Zhu ◽  
Yangong Liu ◽  
Mingqi Zheng ◽  
...  
Keyword(s):  
Potassium Channel ◽  
Expression System ◽  
Hek293 Cells ◽  
Herg Channel ◽  
Delayed Rectifier ◽  
Down Regulation ◽  
Channel Current ◽  
Activation Gating ◽  
Delayed Rectifier Potassium Channel ◽  
Rectifier Potassium Channel

Abstract Gemcitabine is an antineoplastic drug commonly used in the treatment of several types of cancers including pancreatic cancer and non–small cell lung cancer. Although gemcitabine-induced cardiotoxicity is widely recognized, the exact mechanism of cardiac dysfunction causing arrhythmias remains unclear. The objective of this study was to electrophysiologically evaluate the proarrhythmic cardiotoxicity of gemcitabine focusing on the human rapid delayed rectifier potassium channel, hERG channel. In heterologous expression system in HEK293 cells, hERG channel current (IhERG) was reduced by gemcitabine when applied for 24 h but not immediately after the application. Gemcitabine modified the activation gating properties of the hERG channel toward the hyperpolarization direction, while inactivation, deactivation or reactivation gating properties were unaffected by gemcitabine. When gemcitabine was applied to hERG-expressing HEK293 cells in combined with tunicamycin, an inhibitor of N-acetylglucosamine phosphotransferase, gemcitabine was unable to reduce IhERG or shift the activation properties toward the hyperpolarization direction. Our results suggest the possible mechanism of arrhythmias caused by gemcitabine revealing a down-regulation of IhERG through the post-translational glycosylation disruption that alters the electrical excitability of cells.

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