- Peptide (C)TASEHSREPSAAGRLSD, corresponding to amino acid residues 465-481 of rat NaV1.1 (Accession P04774). Intracellular loop between domains I and II.
- Rat and mouse brain lysates (1:200-1:1000).
- Western blot analysis of rat brain (lanes 1 and 3) and mouse brain (lanes 2 and 4) lysates:1,2. Guinea pig Anti-SCN1A (NaV1.1) Antibody (#AGP-043), (1:200).
3,4. Guinea pig Anti-SCN1A (NaV1.1) Antibody, preincubated with SCN1A/Nav1.1 Blocking Peptide (#BLP-SC001).
- Following a broad screen of secondary antibodies, the following was used for this application: #106-035-006 (Jackson ImmunoResearch).
Voltage-gated Na+ channels (NaV) are essential for the generation of action potentials and for cell excitability1. NaV channels are activated in response to depolarization and selectively allow the flow of Na+ ions. To date, nine NaV α subunits have been cloned and named NaV1.1-NaV1.94-5. The NaV channels are classified into two groups according to their sensitivity to tetrodotoxin (TTX): TTX-sensitive (NaV1.1, NaV1.2, NaV1.3, NaV1.4, NaV1.6 and NaV1.7) and TTX-resistant (NaV1.5, NaV1.8 and NaV1.9)2-3.
Mammalian sodium channels are heterotrimers composed of a central, pore-forming α subunit and two auxiliary β subunits. The expression of the α subunit isoform is developmentally regulated and tissue specific. Na+ channels in the adult central nervous system and heart contain β1 through β4 subunits, whereas Na+ channels in adult skeletal muscle have only the β1 subunit6,7.
NaV1.1, also referred to as SCN1A, is a tetrodotoxin-sensitive channel and is broadly expressed in neurons7.
Mutations in NaV1.1 are associated with at least two forms of epilepsy. Gain-of-function missense mutations are a primary cause of generalized epilepsy with febrile seizures plus (GEFS+). Loss-of-function mutations cause severe myoclonic epilepsy of infancy (SMEI)8,9.