ArticleThe Journal of general physiology2006
Differential sialylation modulates voltage-gated Na+ channel gating throughout the developing myocardium.
Article in The Journal of general physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- Sialylation in the nervous system: Functions and mechanisms.The Journal of biological chemistry · 2026Review
- Isoform-specific N-linked glycosylation of NaV channel α-subunits alters β-subunit binding sites.The Journal of general physiology · 2025Article
- Cardiomyocyte Reduction of Hybrid/Complex N-Glycosylation in the Adult Causes Heart Failure With Reduced Ejection Fraction in the Absence of Cellular Remodeling.Journal of the American Heart Association · 2024Article
- ST8Sia2 polysialyltransferase protects against infection by Trypanosoma cruzi.PLoS neglected tropical diseases · 2024Article
- Membrane polarization at the excitation threshold induced by external electric fields in cardiomyocytes of rats at different developmental stages.Medical & biological engineering & computing · 2023Article
- Alterations in mitochondrial protein glycosylation in myocardial ischaemia reperfusion injury.Biochemistry and biophysics reports · 2023Article
- Genomic and Non-Genomic Regulatory Mechanisms of the Cardiac Sodium Channel in Cardiac Arrhythmias.International journal of molecular sciences · 2022Review
- Cardio-Oncology: Understanding the Intersections Between Cardiac Metabolism and Cancer Biology.JACC. Basic to translational science · 2021Review
- Importance of evaluating protein glycosylation in pluripotent stem cell-derived cardiomyocytes for research and clinical applications.Pflugers Archiv : European journal of physiology · 2021Review
- Calmodulin binds to the N-terminal domain of the cardiac sodium channel NaChannels (Austin, Tex.) · 2020Article
- Reference glycan structure libraries of primary human cardiomyocytes and pluripotent stem cell-derived cardiomyocytes reveal cell-type and culture stage-specific glycan phenotypes.Journal of molecular and cellular cardiology · 2020Article
- A small-molecule LF3 abrogates β-catenin/TCF4-mediated suppression of NaJournal of molecular and cellular cardiology · 2019Article
- Cationic Modulation of Voltage-Gated Sodium Channel (Nav1.5): Neonatal Versus Adult Splice Variants-1. Monovalent (HBioelectricity · 2019Article
- Reduced myocyte complex N-glycosylation causes dilated cardiomyopathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- N-glycan content modulates kainate receptor functional properties.The Journal of physiology · 2017Article
- Aberrant sialylation causes dilated cardiomyopathy and stress-induced heart failure.Basic research in cardiology · 2016Article
- Voltage-Gated Na+ Channels: Not Just for Conduction.Cold Spring Harbor perspectives in biology · 2016Review
- Cardiac Na Channels: Structure to Function.Current topics in membranes · 2016Article
- Sialic acids attached to N- and O-glycans within the Nav1.4 D1S5-S6 linker contribute to channel gating.Biochimica et biophysica acta · 2015Article
- Reduced sialylation impacts ventricular repolarization by modulating specific K+ channel isoforms distinctly.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated sodium channel function from neonatal and adult rat cardiomyocytes was measured and compared. Channels from neonatal ventricles required an approximately 10 mV greater depolarization for voltage-dependent gating events than did channels from neonatal atria and adult atria and ventricles. We questioned whether such gating shifts were due to developmental and/or chamber-dependent changes in channel-associated functional sialic acids. Thus, all gating characteristics for channels from neonatal atria and adult atria and ventricles shifted significantly to more depolarized potentials after removal of surface sialic acids. Desialylation of channels from neonatal ventricles did not affect channel gating. After removal of the complete surface N-glycosylation structures, gating of channels from neonatal atria and adult atria and ventricles shifted to depolarized potentials nearly identical to those measured for channels from neonatal ventricles. Gating of channels from neonatal ventricles were unaffected by such deglycosylation. Immunoblot gel shift analyses indicated that voltage-gated sodium channel alpha subunits from neonatal atria and adult atria and ventricles are more heavily sialylated than alpha subunits from neonatal ventricles. The data are consistent with approximately 15 more sialic acid residues attached to each alpha subunit from neonatal atria and adult atria and ventricles. The data indicate that differential sialylation of myocyte voltage-gated sodium channel alpha subunits is responsible for much of the developmental and chamber-specific remodeling of channel gating observed here. Further, cardiac excitability is likely impacted by these sialic acid-dependent gating effects, such as modulation of the rate of recovery from inactivation. A novel mechanism is described by which cardiac voltage-gated sodium channel gating and subsequently cardiac rhythms are modulated by changes in channel-associated sialic acids.
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