Guinea pig Anti-SCN1A (NaV1.1) Antibody

Antibodies

Brain type I sodium channel, BI, Sodium channel protein type 1 subunit α

Shipped at room temperature. Product as supplied can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C

Lyophilized powder

Brain type I sodium channel, BI, Sodium channel protein type 1 subunit α - A Guinea Pig Polyclonal Antibody to SCN1A (NaV1.1) Channel

Mouse, human - identical

Confirmed by amino acid analysis and mass spectrometry

0.8 mg/ml

Intracellular loop between domains I and II

Rat

41116161

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.