ArticleJournal of molecular and cellular cardiology2008
Kv4.3 is not required for the generation of functional Ito,f channels in adult mouse ventricles.
Article in Journal of molecular and cellular cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Pacemaking in the lymphatic system.The Journal of physiology · 2026Review
- Voltage-dependent potassium channel regulatory subunits in the immune system.Biophysical reviews · 2026Review
- A dominant negative Kcnd3 F227del mutation in mice causes spinocerebellar ataxia type 22 (SCA22) by impairing ER and Golgi functioning.The Journal of pathology · 2025Article
- Obesity-induced activation of NADPH oxidase 2 prolongs cardiac repolarization via inhibiting K+ currents.PloS one · 2024Article
- Cardiac muscle-restricted partial loss of Nos1ap expression has limited but significant impact on electrocardiographic features.G3 (Bethesda, Md.) · 2023Article
- A Common East Asian aldehyde dehydrogenase 2*2 variant promotes ventricular arrhythmia with chronic light-to-moderate alcohol use in mice.Communications biology · 2023Article
- Vulnerability of Human Cerebellar Neurons to Degeneration in Ataxia-Causing Channelopathies.Frontiers in systems neuroscience · 2022Review
- SUMOylation of the Kv4.2 Ternary Complex Increases Surface Expression and Current Amplitude by Reducing Internalization in HEK 293 Cells.Frontiers in molecular neuroscience · 2021Article
- Kv4.3 expression abrogates and reverses norepinephrine-induced myocyte hypertrophy by CaMKII inhibition.Journal of molecular and cellular cardiology · 2019Article
- Novel Features and Abnormal Pattern of Cerebral Glucose Metabolism in Spinocerebellar Ataxia 19.Cerebellum (London, England) · 2018Article
- Purkinje Cell Signaling Deficits in Animal Models of Ataxia.Frontiers in synaptic neuroscience · 2018Review
- KFrontiers in physiology · 2018Article
- Early remodeling of repolarizing KJournal of molecular and cellular cardiology · 2017Article
- KChIP2 genotype dependence of transient outward current (Ito) properties in cardiomyocytes isolated from male and female mice.PloS one · 2017Article
- Molecular Basis of Functional Myocardial Potassium Channel Diversity.Cardiac electrophysiology clinics · 2016Review
- IA Channels Encoded by Kv1.4 and Kv4.2 Regulate Circadian Period of PER2 Expression in the Suprachiasmatic Nucleus.Journal of biological rhythms · 2015Article
- Reduced sialylation impacts ventricular repolarization by modulating specific K+ channel isoforms distinctly.The Journal of biological chemistry · 2015Article
- Kv4.3-Encoded Fast Transient Outward Current Is Presented in Kv4.2 Knockout Mouse Cardiomyocytes.PloS one · 2015Article
- Calcineurin-dependent ion channel regulation in heart.Trends in cardiovascular medicine · 2014Review
- Stabilization of Kv4 protein by the accessory K(+) channel interacting protein 2 (KChIP2) subunit is required for the generation of native myocardial fast transient outward K(+) currents.The Journal of physiology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Accumulated evidence suggests that the heteromeric assembly of Kv4.2 and Kv4.3 alpha-subunits underlies the fast transient Kv current (I(to,f)) in rodent ventricles. Recent studies, however, demonstrated that the targeted deletion of Kv4.2 results in the complete elimination of I(to,f) in adult mouse ventricles, revealing an essential role for the Kv4.2 alpha-subunit in the generation of mouse ventricular I(to,f) channels. The present study was undertaken to investigate directly the functional role of Kv4.3 by examining the effects of the targeted disruption of the KCND3 (Kv4.3) locus. Mice lacking Kv4.3 (Kv4.3-/-) appear indistinguishable from wild-type control animals, and no structural or functional abnormalities were evident in Kv4.3-/- hearts. Voltage-clamp recordings revealed that functional I(to,f) channels are expressed in Kv4.3-/- ventricular myocytes, and that mean I(to,f) densities are similar to those recorded from wild-type cells. In addition, I(to,f) properties (inactivation rates, voltage dependences of inactivation and rates of recovery from inactivation) in Kv4.3-/- and wild-type mouse ventricular myocytes were indistinguishable. Quantitative RT-PCR and Western blot analyses did not reveal any measurable changes in the expression of Kv4.2 or the Kv channel interacting protein (KChIP2) in Kv4.3-/- ventricles. Taken together, the results presented here suggest that, in contrast with Kv4.2, Kv4.3 is not required for the generation of functional mouse ventricular I(to,f) channels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.