ArticleThe Journal of physiology2003
Molecular dissection of the inward rectifier potassium current (IK1) in rabbit cardiomyocytes: evidence for heteromeric co-assembly of Kir2.1 and Kir2.2.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 123 citations in OpenAlex.
- Magnesium and Cardiac Arrythmias: An Overlooked Guardian of Electrical Stability.Cardiology research · 2026Review
- The network of cardiac KNaunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Modulation of cardiac voltage-activated KLife sciences · 2022Article
- Calcium Signaling in Cardiomyocyte Function.Cold Spring Harbor perspectives in biology · 2020Review
- Canonical Wnt signaling promotes pacemaker cell specification of cardiac mesodermal cells derived from mouse and human embryonic stem cells.Stem cells (Dayton, Ohio) · 2020Article
- Engineered Cardiac Pacemaker Nodes Created by TBX18 Gene Transfer Overcome Source-Sink Mismatch.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019Article
- Inward rectifying potassium currents resolved into components: modeling of complex drug actions.Pflugers Archiv : European journal of physiology · 2018Article
- Influence of Continuous Training on Atrial Myocytes ICardiology research and practice · 2018Article
- Functional expression and pharmaceutical efficacy of cardiac-specific ion channels in human embryonic stem cell-derived cardiomyocytes.Scientific reports · 2017Article
- Inhibition of inwardly rectifying Kir2.x channels by the novel anti-cancer agent gambogic acid depends on both pore block and PIPNaunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Role of plasma membrane-associated AKAPs for the regulation of cardiac INaunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Transmural gradients in ion channel and auxiliary subunit expression.Progress in biophysics and molecular biology · 2016Review
- The Effects of Puerarin on Rat Ventricular Myocytes and the Potential Mechanism.Scientific reports · 2016Article
- Inhibition of Cardiac Kir Current (IK1) by Protein Kinase C Critically Depends on PKCβ and Kir2.2.PloS one · 2016Article
- Pacing the Heart with Genes: Recent Progress in Biological Pacing.Current cardiology reports · 2015Review
- Regional variation of the inwardly rectifying potassium current in the canine heart and the contributions to differences in action potential repolarization.Journal of molecular and cellular cardiology · 2015Article
- Channelopathies of skeletal muscle excitability.Comprehensive Physiology · 2015Review
- Cardiac ion channels.Channels (Austin, Tex.) · 2015Review
- Class III antiarrhythmic drug dronedarone inhibits cardiac inwardly rectifying Kir2.1 channels through binding at residue E224.Naunyn-Schmiedeberg's archives of pharmacology · 2014Article
- Mitochondria and arrhythmias.Free radical biology & medicine · 2014Review
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac inward rectifier K+ currents (IK1) play an important role in maintaining resting membrane potential and contribute to late phase repolarization. Members of the Kir2.x channel family appear to encode for IK1. The purpose of this study was to determine the molecular composition of cardiac IK1 in rabbit ventricle. Western blots revealed that Kir2.1 and Kir2.2, but not Kir2.3, are expressed in rabbit ventricle. Culturing rabbit myocytes resulted in an approximately 50% reduction of IK1 density after 48 or 72 h in culture which was associated with an 80% reduction in Kir2.1, but no change in Kir2.2, protein expression. Dominant-negative (DN) constructs of Kir2.1, Kir2.2 and Kir2.3 were generated and tested in tsA201 cells. Adenovirus-mediated over-expression of Kir2.1dn, Kir2.2dn or Kir2.1dn plus Kir2.2dn in cultured rabbit ventricular myocytes reduced IK1 density equally by 70% 72 h post-infection, while AdKir2.3dn had no effect, compared to green fluorescent protein (GFP)-infected myocytes. Previous studies indicate that the [Ba2+] required for half-maximum block (IC50) differs significantly between Kir2.1, Kir2.2 and Kir2.3 channels. The dependence of IK1 on [Ba2+] revealed a single binding isotherm which did not change with time in culture. The IC50 for block of IK1 was also unaffected by expression of the different DN genes after 72 h in culture. Taken together, these results demonstrate functional expression of Kir2.1 and Kir2.2 in rabbit ventricular myocytes and suggest that macroscopic IK1 is predominantly composed of Kir2.1 and Kir2.2 heterotetramers.
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