IndraLab

Statements

SCN8A activates sodium(1+). 13 / 13
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"FHF2 isoforms differentially regulate Nav1.6 mediated resurgent sodium currents in dorsal root ganglion neurons."
27999940
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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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"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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"Scn8a is a gene that encodes an alpha subunit of the voltage-gated sodium channel Nav1.6 which mediates voltage-dependent sodium ion permeability of excitable membranes."
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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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"The mutation in Scn8a results in a gain-of-function effect in the Nav1.6 sodium channel, causing an increase in sodium influx into neurons [116]."
39452036
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"In murine cochlear spiral ganglion, the Nav1.6‐specific blocker 4.9‐ah‐TTX reduced the amplitude of sodium‐activated currents during depolarization by 70%, suggesting a similarly significant contribution of the Nav1.6 channel in forming sodium currents in the ganglionic neuron."
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"In these double Gars/Scn8a heterozygotes, reduced axon diameter and impaired sodium currents, presumably causing depolarization problems, synergize to produce more severe reductions in nerve conduction velocity and NMJ defects (Morelli et al., 2017)."
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"Endogenous sodium currents are mainly mediated by Nav1.6 and Nav1.7, but also Nav1.1, Nav1.2, Nav1.3 and Nav1.9 at low levels ( Lee et al., 2019 )."
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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)."
27270488
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"23 , 24 Resurgent sodium currents mediated by Nav1.6 may be important contributors to burst firing."
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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