NaV1.1 | sodium voltage-gated channel alpha subunit 1

Sodium channels


Alpha subunits consist of four homologous domains (I-IV) with six transmembrane alpha helices (S1–S6) and a pore-forming loop. One a subunit may associate with 1 or 2 b subunits to make up the channel.

NaV1.1: Background Information

NaV1.1 is a voltage-gated ion channel essential for the generation and propagation of action potentials, and is expressed in nerve, glial cells and muscle. In neurons NaV1.1 is presumably involved in propagating synaptic signals from dendrites to soma and in integration of electrical signals within the soma prior to the initiation of axonal action potentials. NaV1.1 is the primary voltage-gated Na+ channel in several clases of GABAergic interneurons, and its reduced activity leads to reduced excitability and decreased GABAergic tone. NaV1.1 is TTX-sensitive.


Human Protein:
UniProt P35498

Brain (neurons, glia)

Function/ Application:
Excitability of neurons, generation of action potentials

Pain, epilepsy (SMEI, GEFS+), migraine (FHM3), Rasmussen's encephalitis, autism, Dravet syndrome, Lennox-Gastaut syndrome, Panayiotopoulos syndrome, Doose syndrome

Accessory subunits:
b1, b2, b3, b4

Alpha-1 syntrophin, β1 subunit, β2 subunit, calmodulin, Ca2+, FHF4

Tetrodotoxin, ATX-II, Bc-III, AFT-II, Lidocaine

Patch Clamp: whole cell, room temperature, State- and use-dependence

NaV channel analysis requires GigaOhm seals and a stable and low access resistance

Recommended Reviews:
International Union of Pharmacology. XLVII. Nomenclature and Structure-Function Relationships of Voltage-Gated Sodium Channels. Pharmacol Rev 57: 397–409, Catterall, et al. 2005 


03.11.2016 | External Webinar: Accelerating Ion Channel Characterization and New Drug Candidate Identification

icon sp96   SyncroPatch 384PE

This webinar will show high-throughput functional annotation of human ion channel variants associated with excitation disorders will be described along with use of the Syncropatch 384PE to measure subtype selective activation of KV7 potassium channels as well as inhibition of voltage gated sodium channels like NaV1.7, NaV1.1, and NaV1.5.
Organisation: Icagen Inc.


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