IndraLab

Statements

SCN8A activates sodium(1+). 8 / 8
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"SCN8A encephalopathy is a newly defined EE caused by de novo mutations of the gene SCN8A encoding the sodium channel Na v 1.6 (OMIM # 614558)."
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"PHN-associated VZV sodium current increases were therefore mediated in part by the Nav 1.6 and Nav 1.7 sodium ion channels."
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"Based on analysis of cells from mice with a Scn8a null mutation, Scn8a channels appear to contribute significantly to total sodium current in both in P10-P14 Purkinje cells (approximately 40%; [21]) and cultured P7-P8 spinal motoneurons (approximately 70% [K.D. Garcia, L.K. Sprunger, M.H. Meisler, K.G. Beam, The sodium channel Scn8a is the major contributor to the postnatal developmental increase of sodium current density in spinal motoneurons, J. Neurosci."
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"FHF2 isoforms differentially regulate Nav1.6 mediated resurgent sodium currents in dorsal root ganglion neurons."
27999940
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"NaV1.6 dysregulation within myocardial T-tubules by D96V calmodulin enhances proarrhythmic sodium and calcium mishandling."
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"The Nav1.6 channel blocker, 4,9-anhydrotetrodotoxin, reduced a component of sodium current in immature and mature calyces."
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"Functional studies suggest that SCN8A missense mutations may cause impaired channel inactivation and persistent sodium current, which may increase neuronal excitability and firing."
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"Three recognized sodium channel gene EEs are caused by mutations in SCN8A, SCN1A (Dravet syndrome), SCN2A, and SCN8A."
27270488