ArticleThe Journal of clinical investigation2009
Endocytic control of ion channel density as a target for cardiovascular disease.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022Review
- Ion Channel Expression in Human Melanoma Samples: In Silico Identification and Experimental Validation of Molecular Targets.Cancers · 2019Article
- Plasticity of sarcolemmal KATP channel surface expression: relevance during ischemia and ischemic preconditioning.American journal of physiology. Heart and circulatory physiology · 2016Article
- MiRNA and TF co-regulatory network analysis for the pathology and recurrence of myocardial infarction.Scientific reports · 2015Article
- Transient receptor potential melastatin 4 and cell death.Pflugers Archiv : European journal of physiology · 2012Review
- hERG K+ channel-associated cardiac effects of the antidepressant drug desipramine.Naunyn-Schmiedeberg's archives of pharmacology · 2011Article
- Multiple mechanisms of hERG liability: K+ current inhibition, disruption of protein trafficking, and apoptosis induced by amoxapine.Naunyn-Schmiedeberg's archives of pharmacology · 2010Article
- Interaction of local anesthetics with the K (+) channel pore domain: KcsA as a model for drug-dependent tetramer stability.Channels (Austin, Tex.)Article
- Basal protein kinase Cδ activity is required for membrane localization and activity of TRPM4 channels in cerebral artery smooth muscle cells.Channels (Austin, Tex.)Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Ion channels encoded by the human ether-a-go-go-related gene (HERG) give rise to the rapidly activating delayed rectifier K+ current (IKr), the perturbation of which causes ventricular arrhythmias associated with inherited and acquired long QT syndrome. Electrolyte imbalances, such as reduced serum K+ levels (hypokalemia), also trigger these potentially fatal arrhythmias. In this issue of the JCI, Guo et al. report that physiological levels of serum K+ are required to maintain normal HERG surface density in HEK 293 cells and IKr in rabbit cardiomyocytes. They found that hypokalemia evoked HERG channel ubiquitination, enhanced internalization via endocytosis, and ultimately degradation at the lysosome, thus identifying unbridled turnover as a mechanism of hypokalemia-induced arrhythmia. But too little channel turnover can also cause disease, as suggested by Kruse et al. in a study also in this issue. The authors identified mutations in TRPM4--a nonselective cation channel--in a large family with progressive familial heart block type I and showed that these mutations prevented channel internalization (see the related articles beginning on pages 2745 and 2737, respectively).
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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.