ArticleThe Journal of biological chemistry2013
[Ca2+]i elevation and oxidative stress induce KCNQ1 protein translocation from the cytosol to the cell surface and increase slow delayed rectifier (IKs) in cardiac myocytes.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- Dysregulated Cell Homeostasis and miRNAs in Human iPSC-Derived Cardiomyocytes from a Propionic Acidemia Patient with Cardiomyopathy.International journal of molecular sciences · 2023Article
- Outlining cardiac ion channel protein interactors and their signature in the human electrocardiogram.Nature cardiovascular research · 2023Article
- Myocardial TRPC6-mediated ZnNature communications · 2022Article
- Delayed KCNQ1/KCNE1 assembly on the cell surface helps IThe Journal of physiology · 2021Article
- Mechanisms and Regulation of Cardiac CaInternational journal of molecular sciences · 2021Review
- β-Adrenergic control of sarcolemmal CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- The unconventional biogenesis of Kv7.1-KCNE1 complexes.Science advances · 2020Article
- β-adrenergic-mediated dynamic augmentation of sarcolemmal CaThe Journal of physiology · 2019Article
- Chronic in vivo angiotensin II administration differentially modulates the slow delayed rectifier channels in atrial and ventricular myocytes.Heart rhythm · 2019Article
- Cardiolipotoxicity, Inflammation, and Arrhythmias: Role for Interleukin-6 Molecular Mechanisms.Frontiers in physiology · 2018Review
- cAMP-dependent regulation ofThe Journal of general physiology · 2017Article
- Adult Ventricular Myocytes Segregate KCNQ1 and KCNE1 to Keep theCirculation. Arrhythmia and electrophysiology · 2017Article
- Quantitative analysis of the CaThe Journal of physiology · 2017Article
- Potassium channels in the heart: structure, function and regulation.The Journal of physiology · 2017Review
- Adrenergic Stress Protection of Human iPS Cell-Derived Cardiomyocytes by Fast KFrontiers in physiology · 2017Article
- JPH-2 interacts with Cai-handling proteins and ion channels in dyads: Contribution to premature ventricular contraction-induced cardiomyopathy.Heart rhythm · 2016Article
- Article
- Probing binding sites and mechanisms of action of an I(Ks) activator by computations and experiments.Biophysical journal · 2015Article
- Article
- Stoichiometry of the cardiac IKs complex.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Our goals are to simultaneously determine the three-dimensional distribution patterns of KCNQ1 and KCNE1 in cardiac myocytes and to study the mechanism and functional implications for variations in KCNQ1/KCNE1 colocalization in myocytes. We monitored the distribution patterns of KCNQ1, KCNE1, and markers for subcellular compartments/organelles using immunofluorescence/confocal microscopy and confirmed the findings in ventricular myocytes by directly observing fluorescently tagged KCNQ1-GFP and KCNE1-dsRed expressed in these cells. We also monitored the effects of stress on KCNQ1-GFP and endoplasmic reticulum (ER) remodeling during live cell imaging. The data showed that 1) KCNE1 maintained a stable cell surface localization, whereas KCNQ1 exhibited variations in the cytosolic compartment (striations versus vesicles) and the degree of presence on the cell surface; 2) the degree of cell surface KCNQ1/KCNE1 colocalization was positively correlated with slow delayed rectifier (IKs) current density; 3) KCNQ1 and calnexin (an ER marker) shared a cytosolic compartment; and 4) in response to stress ([Ca(2+)]i elevation, oxidative overload, or AT1R stimulation), KCNQ1 exited the cytosolic compartment and trafficked to the cell periphery in vesicles. This was accompanied by partial ER fragmentation. We conclude that the cellular milieu regulates KCNQ1 distribution in cardiac myocytes and that stressful conditions can increase IKs by inducing KCNQ1 movement to the cell surface. This represents a hitherto unrecognized mechanism by which IKs fulfills its function as a repolarization reserve in ventricular myocytes.
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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.