ArticleJournal of cell science2014
Tuning the electrical properties of the heart by differential trafficking of KATP ion channel complexes.
Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 54 citations in OpenAlex.
- 14-3-3 proteins: Regulators of cardiac excitation-contraction coupling and stress responses.The Journal of physiology · 2026Review
- Muscle fatigue arising intrinsically from SUR2- but not Kir6.1-dependent gain-of-function in Cantu syndrome mice.The Journal of general physiology · 2025Article
- 14-3-3 promotes sarcolemmal expression of cardiac CaProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Do We Need a New Hypothesis for KATP Closure in β-Cells? Distinguishing the Baby From the Bathwater.Diabetes · 2024Article
- Article
- 14-3-3 proteins regulate cullin 7-mediated Eag1 degradation.Cell & bioscience · 2023Article
- Rab35 GTPase positively regulates endocytic recycling of cardiac KChannels (Austin, Tex.) · 2022Article
- Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022Review
- 14-3-3 protein regulation of excitation-contraction coupling.Pflugers Archiv : European journal of physiology · 2022Review
- Genomic and Non-Genomic Regulatory Mechanisms of the Cardiac Sodium Channel in Cardiac Arrhythmias.International journal of molecular sciences · 2022Review
- Distributed synthesis of sarcolemmal and sarcoplasmic reticulum membrane proteins in cardiac myocytes.Basic research in cardiology · 2021Article
- Paeonol promotes Opa1-mediated mitochondrial fusion via activating the CK2α-Stat3 pathway in diabetic cardiomyopathy.Redox biology · 2021Article
- Complex consequences of Cantu syndrome SUR2 variant R1154Q in genetically modified mice.JCI insight · 2021Article
- Cardiac T-Tubule cBIN1-Microdomain, a Diagnostic Marker and Therapeutic Target of Heart Failure.International journal of molecular sciences · 2021Review
- Genetic Discovery of ATP-Sensitive KCirculation. Arrhythmia and electrophysiology · 2019Review
- Dual RXR motifs regulate nerve growth factor-mediated intracellular retention of the delta opioid receptor.Molecular biology of the cell · 2019Article
- Directing Traffic: Regulation of COPI Transport by Post-translational Modifications.Frontiers in cell and developmental biology · 2019Review
- Report on the Ion Channel Symposium : Organized by the German Cardiac Society Working Group on Cellular Electrophysiology (AG 18).Herzschrittmachertherapie & Elektrophysiologie · 2018Review
- Axial Tubule Junctions Activate Atrial CaFrontiers in physiology · 2018Article
- Cardiac T-Tubule Microanatomy and Function.Physiological reviews · 2017Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
The copy number of membrane proteins at the cell surface is tightly regulated. Many ion channels and receptors present retrieval motifs to COPI vesicle coats and are retained in the early secretory pathway. In some cases, the interaction with COPI is prevented by binding to 14-3-3 proteins. However, the functional significance of this antagonism between COPI and 14-3-3 in terminally differentiated cells is unknown. Here, we show that ATP-sensitive K(+) (KATP) channels, which are composed of Kir6.2 and SUR1 subunits, are stalled in the Golgi complex of ventricular, but not atrial, cardiomyocytes. Upon sustained β-adrenergic stimulation, which leads to activation of protein kinase A (PKA), SUR1-containing channels reach the plasma membrane of ventricular cells. We show that PKA-dependent phosphorylation of the C-terminus of Kir6.2 decreases binding to COPI and, thereby, silences the arginine-based retrieval signal. Thus, activation of the sympathetic nervous system releases this population of KATP channels from storage in the Golgi and, hence, might facilitate the adaptive response to metabolic challenges.
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Identifiers
What Socratic holds
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 Socratic graph.