Scn1b cDNA ORF clone, Mus musculus(house mouse)

Genetic Causes of Generalized Epilepsies.
Helbig I
Seminars in neurology35(3)288-92(2015 Jun)

Na Channel ? Subunits: Overachievers of the Ion Channel Family.
Brackenbury WJ, Isom LL
Frontiers in pharmacology253(2011)

This study demonstrated that the sodium channel beta1 subunit proteins encoded by this mutant gene are expressed at the surface of neuronal cell bodies.
Title: ?1-C121W Is Down But Not Out: Epilepsy-Associated Scn1b-C121W Results in a Deleterious Gain-of-Function.

Study showed that Scn1b is widely expressed at axon initial segments across the mouse brain, there is considerable heterogeneity in the proportion of Scn1b-positive neurons and the amount of expression between and within brain regions
Title: Sodium channel ?1 subunit localizes to axon initial segments of excitatory and inhibitory neurons and shows regional heterogeneity in mouse brain.

Loss of Scn1b caused increased amplitude of tetrodotoxin-sensitive INa, delayed after-depolarizations, triggered beats, changed Ca2+ transients,and susceptibility ventricular arrhythmias.
Title: Scn1b deletion leads to increased tetrodotoxin-sensitive sodium current, altered intracellular calcium homeostasis and arrhythmias in murine hearts.

Scn1b mutant subicular and layer 2/3 pyramidal neurons had increased action potential firing rates, presumably as a consequence of their increased input resistance
Title: Reduced dendritic arborization and hyperexcitability of pyramidal neurons in a Scn1b-based model of Dravet syndrome.

beta1-beta3 is more likely to form a di-polymer than beta1-beta1 based on molecular interaction analysis, including potential energy analysis
Title: Study of the residues involved in the binding of ?1 to ?3 subunits in the sodium channel.