Nav1.1 Antibody
(Synonyms: Sodium channel protein type 1 subunit alpha, Sodium channel protein brain I subunit alpha, Sodium channel protein type I subunit alpha, Voltage-gated sodium channel subunit alpha Nav1.1, Scn1a)Nav1.1 Antibody is a Rabbit-derived and non-conjugated IgG Polyclonal antibody, targeting to Nav1.1.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, FC, ELISA
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Reactivity :
Human
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Formulation:
Supplied in PBS(pH 7.4), 30% glycerol, and 0.01% sodium azide.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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FC
FC: Flow Cytometry
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ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|
| Dilution Ratio | 1:500-1000 | 1:10-50 | 1:3000-5000 |
Product Details
Nav1.1 Antibody is a Rabbit-derived and non-conjugated IgG Polyclonal antibody, targeting to Nav1.1.
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Host Rabbit
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Clonality Polyclonal
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Species ReactivityHuman
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Observed Molecular WeightObserved band size: 260 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 228 kDa
Synthetic peptide of human Nav1.1 (Central region ).
Endogenous
Affinity purified
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS(pH 7.4), 30% glycerol, and 0.01% sodium azide.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
NaV1.1, encoded by SCN1A, supports neuronal action-potential signaling and is closely linked to epilepsy biology[1]. Mechanistically, NaV1.1 localizes to axons of parvalbumin-positive inhibitory interneurons, positioning this channel within GABAergic circuit control[2]. In Dravet syndrome models, Scn1a dysfunction reduces sodium current in GABAergic interneurons, weakens inhibitory output, and promotes seizure susceptibility[3][4][5]. Compared with NaV1.6, NaV1.1 represents the inhibitory side of neuronal excitation-inhibition balance, whereas NaV1.6 overactivity supports excitatory epileptic mechanisms[61]. For experimental applications, selective NaV1.1 activation with Hm1a restored inhibitory interneuron function and reduced seizures in Dravet syndrome mice, while small-molecule NaV1.1 activators increased fast-spiking interneuron excitability and GABAergic transmission[7][8].
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Subcellular Localization
Cell membrane; Multi-pass membrane protein
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Isoforms & Post-Translational Modification
Nav1.1 has three isomers: P35498-1: 2009 amino acids, molecular weight 228,972 Da (predicted); P35498-2: 1998 amino acids, molecular weight 227,789 Da (predicted); P35498-3: 1981 amino acids, molecular weight 226,174 Da (predicted).
Phosphorylation of the Ser-1516 site in the highly conserved cytoplasmic loop by PKC slows down the inactivation of sodium channels and reduces peak sodium current. -
Subunit
The Nav1.1 voltage-gated sodium channel consists of an ion-conducting alpha subunit SCN1A which is functional on its own regulated by one or more beta-1 (SCN1B), beta-2 (SCN2B), beta-3 (SCN3B) and beta-4 (SCN4B) subunits. SCN1B and SCN3B are non-covalently associated with SCN1A. SCN2B and SCN4B are disulfide-linked to SCN1A. SCN1B regulates both the expression at the plasma membrane and the voltage dependence of Nav1.1 inactivation. SCN3B and SCN4B reduce Nav1.1 conductance. Interacts with FGF13; regulates the steady-state inactivation of Nav.1.1.
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SwissProt ID
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Synonyms
Sodium channel protein type 1 subunit alpha, Sodium channel protein brain I subunit alpha, Sodium channel protein type I subunit alpha, Voltage-gated sodium channel subunit alpha Nav1.1, Scn1a
Documentation
References
[1]. Catterall WA, et al. NaV1.1 channels and epilepsy. J Physiol. 2010 Jun 1;588(Pt 11):1849-59. [Content Brief]
[2]. Ogiwara I, et al. Nav1.1 localizes to axons of parvalbumin-positive inhibitory interneurons: a circuit basis for epileptic seizures in mice carrying an Scn1a gene mutation. J Neurosci. 2007 May 30;27(22):5903-14. [Content Brief]
[3]. Yu FH, et al. Reduced sodium current in GABAergic interneurons in a mouse model of severe myoclonic epilepsy in infancy. Nat Neurosci. 2006 Sep;9(9):1142-9. [Content Brief]
[4]. Cheah CS, et al. Specific deletion of NaV1.1 sodium channels in inhibitory interneurons causes seizures and premature death in a mouse model of Dravet syndrome. Proc Natl Acad Sci U S A. 2012 Sep 4;109(36):14646-51. [Content Brief]
[5]. Tai C, et al. Impaired excitability of somatostatin- and parvalbumin-expressing cortical interneurons in a mouse model of Dravet syndrome. Proc Natl Acad Sci U S A. 2014 Jul 29;111(30):E3139-48. [Content Brief]
[6]. Weuring WJ, et al. NaV1.1 and NaV1.6 selective compounds reduce the behavior phenotype and epileptiform activity in a novel zebrafish model for Dravet Syndrome. PLoS One. 2020 Mar 5;15(3):e0219106. [Content Brief]
[7]. Richards KL, et al. Selective NaV 1.1 activation rescues Dravet syndrome mice from seizures and premature death. Proc Natl Acad Sci U S A. 2018 Aug 21;115(34):E8077-E8085. [Content Brief]
[8]. Chow CY, et al. A selective NaV 1.1 activator with potential for treatment of Dravet syndrome epilepsy. Biochem Pharmacol. 2020 Nov;181:113991. [Content Brief]
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