Biochemical and Biophysical Research Communications
Regular ArticleModulation of Sodium Current in Mammalian Cells by an Epilepsy-Correlated β1-Subunit Mutation
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Cited by (43)
Voltage-gated sodium channel β subunits: The power outside the pore in brain development and disease
2018, NeuropharmacologyCitation Excerpt :Differential sialic acid modification was also found to affect β2 modulation of Nav1.5 while, in the same study, Nav1.2 was modulated regardless of α subunit sialylation status (Johnson and Bennett, 2006). The epilepsy-linked β1-C121W mutation in Scn1b results in decreased β1 subunit glycosylation and loss of its capacity to modulate VGSC properties and to traffic out of the soma to the axon in mouse neurons (Meadows et al., 2002; Tammaro et al., 2002; Kruger, O'Malley et al., 2016). This raises the possibility that control of glycosylation of β subunits, especially sialyation, may be important in subcellular targeting and α-β subunit association.
Differential gene expression profiles of two excitable rat cell lines after over-expression of WT- and C121W-β1 sodium channel subunits
2015, NeuroscienceCitation Excerpt :To prevent the loss of differentiation potential, cells were not allowed to become confluent. Constructs containing the coding sequence (CDS) of WT- or C121W-NaCh β1 subunit (Tammaro et al., 2002; Moran et al., 2003), fused with the CDS of the enhanced Blue Fluorescent Protein (eBFP) (Baroni et al., 2013, 2014) were used to transfect GH3 and H9C2 cells. Cells were transiently transfected by the calcium phosphate-DNA co-precipitation method (Bacchetti and Graham, 1977) with 6 μg of DNA and were used between 48 and 72 h after transfection.
Identification of an intra-molecular disulfide bond in the sodium channel β1-subunit
2012, Biochemical and Biophysical Research CommunicationsEpileptogenic ion channel mutations: From bedside to bench and, hopefully, back again
2010, Epilepsy ResearchCitation Excerpt :Moreover, some channels have well established accessory subunits, which can be targets of mutations, for example the β1 subunit of Na+ channels or the β4 subunit of high voltage activated (HVA) Ca2+ channels (Table 1), but often their functions have not been clearly identified. For instance, Na+ channel β1 subunit can modulate gating properties and targeting of the principal α subunits, but its properties are highly variable and strictly depend on the expression system used (Isom et al., 1994; Qu et al., 2001; Meadows et al., 2002; Tammaro et al., 2002). β1 subunit mutants can cause GEFS+ or SMEI and show complete loss of function because they cannot modulate α subunits (Meisler and Kearney, 2005; Patino et al., 2009), but their effects on cell excitability are still unclear because those of wild-type β1 are not yet fully understood.
- 1
Present address: Department of Pharmacy and Pharmacology; University of Bath; Bath, UK.
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To whom correspondence and reprint requests should be addressed. Fax: (+39)-010-6475-500. E-mail: [email protected].