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Frank H Yu et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 23(20), 7577-7585 (2003-08-22)
The principal alpha subunit of voltage-gated sodium channels is associated with auxiliary beta subunits that modify channel function and mediate protein-protein interactions. We have identified a new beta subunit termed beta4. Like the beta1-beta3 subunits, beta4 contains a cleaved signal
John Gilchrist et al.
Proceedings of the National Academy of Sciences of the United States of America, 110(51), E5016-E5024 (2013-12-04)
Voltage-gated sodium (Nav) channels are embedded in a multicomponent membrane signaling complex that plays a crucial role in cellular excitability. Although the mechanism remains unclear, β-subunits modify Nav channel function and cause debilitating disorders when mutated. While investigating whether β-subunits
Emeline Bon et al.
Nature communications, 7, 13648-13648 (2016-12-06)
The development of metastases largely relies on the capacity of cancer cells to invade extracellular matrices (ECM) using two invasion modes termed 'mesenchymal' and 'amoeboid', with possible transitions between these modes. Here we show that the SCN4B gene, encoding for
Argelia Medeiros-Domingo et al.
Circulation, 116(2), 134-142 (2007-06-27)
Congenital long-QT syndrome (LQTS) is potentially lethal secondary to malignant ventricular arrhythmias and is caused predominantly by mutations in genes that encode cardiac ion channels. Nearly 25% of patients remain without a genetic diagnosis, and genes that encode cardiac channel
Adélaïde Doray et al.
Cells, 10(7) (2021-07-03)
The SCN4B gene, coding for the NaVβ4 subunit of voltage-gated sodium channels, was recently found to be expressed in normal epithelial cells and down-regulated in several cancers. However, its function in normal epithelial cells has not been characterized. In this
Ruo-Gu Li et al.
International journal of molecular medicine, 32(1), 144-150 (2013-04-23)
Atrial fibrillation (AF) represents the most common form of sustained cardiac arrhythmia and accounts for substantial morbidity and mortality. Mutations in the cardiac sodium channel α, β1, β2 and β3 subunit genes (SCN5A, SCN1B, SCN2B and SCN3B) have been associated
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