ArticleJournal of molecular and cellular cardiology2007
Sodium channel Scn1b null mice exhibit prolonged QT and RR intervals.
Article in Journal of molecular and cellular cardiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.
- Systematic Review of the Genetics of Sudden Unexpected Death in Epilepsy: Potential Overlap With Sudden Cardiac Death and Arrhythmia-Related Genes.Journal of the American Heart Association · 2020Pooled it
- Article
- Heterozygous Loss of Scn1b Results in Concealed Conduction Phenotype Unmasked by Osmotic Stress.bioRxiv : the preprint server for biology · 2026Article
- Unraveling SUDEP: Mechanisms of Seizure-Induced Cardiac and Respiratory Impairment.Epilepsy currents · 2026Article
- Polyphenol-RichPharmaceutics · 2025Article
- Article
- Altered cardiac excitability and arrhythmia in models of SCN1B-linked developmental and epileptic encephalopathy.JCI insight · 2025Article
- Ataxia and cerebellar hypoexcitability in a mouse model of SCN1B-linked Dravet syndrome.JCI insight · 2025Article
- Neuromodulation of voltage-gated sodium channels by Gβ1γ2 subunits: Implications for GNB1-linked encephalopathy.Neurobiology of disease · 2025Article
- Article
- New focus on cardiac voltage-gated sodium channel β1 and β1B: Novel targets for treating and understanding arrhythmias?Heart rhythm · 2025Review
- Decreased ability to manage increases in reactive oxygen species may underlie susceptibility to arrhythmias in mice lackingAmerican journal of physiology. Heart and circulatory physiology · 2024Article
- Sex differences in cardiac mitochondrial respiration and reactive oxygen species production may predisposeJournal of molecular and cellular cardiology plus · 2024Article
- Altered cardiac energetics in mice lacking Scn1b.Cardiovascular research · 2024Article
- The dispensability of 14-3-3 proteins for the regulation of human cardiac sodium channel Nav1.5.PloS one · 2024Article
- Complex Synaptic and Intrinsic Interactions Disrupt Input/Output Functions in the Hippocampus ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- SUMOylation of the cardiac sodium channel NaHeart rhythm · 2023Article
- Differential regulation of cardiac sodium channels by intracellular fibroblast growth factors.The Journal of general physiology · 2023Article
- Cardiac Functional and Structural Abnormalities in a Mouse Model of CDKL5 Deficiency Disorder.International journal of molecular sciences · 2023Article
- Cardiac sodium channel complexes and arrhythmia: structural and functional roles of the β1 and β3 subunits.The Journal of physiology · 2023Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
In neurons, voltage-gated sodium channel beta subunits regulate the expression levels, subcellular localization, and electrophysiological properties of sodium channel alpha subunits. However, the contribution of beta subunits to sodium channel function in heart is poorly understood. We examined the role of beta1 in cardiac excitability using Scn1b null mice. Compared to wildtype mice, electrocardiograms recorded from Scn1b null mice displayed longer RR intervals and extended QT(c) intervals, both before and after autonomic block. In acutely dissociated ventricular myocytes, loss of beta1 expression resulted in a approximately 1.6-fold increase in both peak and persistent sodium current while channel gating and kinetics were unaffected. Na(v)1.5 expression increased in null myocytes approximately 1.3-fold. Action potential recordings in acutely dissociated ventricular myocytes showed slowed repolarization, supporting the extended QT(c) interval. Immunostaining of individual myocytes or ventricular sections revealed no discernable alterations in the localization of sodium channel alpha or beta subunits, ankyrin(B), ankyrin(G), N-cadherin, or connexin-43. Together, these results suggest that beta1 is critical for normal cardiac excitability and loss of beta1 may be associated with a long QT phenotype.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.