Nav1.6 Antibody
(Synonyms: MED, SCN8A, Sodium channel protein type 8 subunit alpha, Sodium channel protein type VIII subunit alpha, Voltage-gated sodium channel subunit alpha Nav1.6)Nav1.6 Antibody is a Rabbit-derived and non-conjugated IgG Polyclonal antibody, targeting to Nav1.6.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, ICC/IF
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS (pH 7.4), containing 30% glycerol, and 0.01% sodium azide.
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
|
ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
|---|---|---|
| Dilution Ratio | 1:1000-2000 | 1:50-200 |
Product Details
Nav1.6 Antibody is a Rabbit-derived and non-conjugated IgG Polyclonal antibody, targeting to Nav1.6.
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Host Rabbit
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Clonality Polyclonal
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Species ReactivityHuman, Mouse, Rat
Synthetic peptide corresponding to the center region of human Nav1.6.
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), containing 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
Nav1.6 is a Pore-forming subunit of a voltage-gated sodium channel complex assuming opened or closed conformations in response to the voltage difference across membranes and through which sodium ions selectively pass along their electrochemical gradient. Contributes to neuronal excitability by regulating action potential threshold and propagation[1][2][3][4][5][6][7][8].
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Subcellular Localization
Cell membrane; Cell projection, axon
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Expression
Tissue_Specificity: Expressed in the hippocampus with increased expression in epileptic tissue compared to normal adjacent tissue (at protein level).
Induction: Up-regulated in the hippocampus after epilepsy. -
Isoforms & Post-Translational Modification
Nav1.May be ubiquitinated by NEDD4L; which would promote its endocytosis
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Subunit
The voltage-sensitive sodium channel consists of an ion-conducting pore-forming alpha subunit regulated by one or more beta-1 (SCN1B), beta-2 (SCN2B), beta-3 (SCN3B) and/or beta-4 (SCN4B) subunits.
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SwissProt ID
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Synonyms
MED, SCN8A, Sodium channel protein type 8 subunit alpha, Sodium channel protein type VIII subunit alpha, Voltage-gated sodium channel subunit alpha Nav1.6
Documentation
References
[1]. Estacion M, et al. A novel de novo mutation of SCN8A (Nav1.6) with enhanced channel activation in a child with epileptic encephalopathy. Neurobiol Dis. 2014 Sep;69:117-23. [Content Brief]
[2]. de Kovel CG, et al. Characterization of a de novo SCN8A mutation in a patient with epileptic encephalopathy. Epilepsy Res. 2014 Nov;108(9):1511-8. [Content Brief]
[3]. Blanchard MG, et al. De novo gain-of-function and loss-of-function mutations of SCN8A in patients with intellectual disabilities and epilepsy. J Med Genet. 2015 May;52(5):330-7. [Content Brief]
[4]. Wagnon JL, et al. Pathogenic mechanism of recurrent mutations of SCN8A in epileptic encephalopathy. Ann Clin Transl Neurol. 2016 Feb;3(2):114-23. [Content Brief]
[5]. Wagnon JL, et al. Partial loss-of-function of sodium channel SCN8A in familial isolated myoclonus. Hum Mutat. 2018 Jul;39(7):965-969. [Content Brief]
[6]. Fry AE, et al. Missense variants in the N-terminal domain of the A isoform of FHF2/FGF13 cause an X-linked developmental and epileptic encephalopathy. Am J Hum Genet. 2021 Jan 7;108(1):176-185. [Content Brief]
[7]. Fan X, et al. Cryo-EM structure of human voltage-gated sodium channel Na(v)1.6. Proc Natl Acad Sci U S A. 2023 Jan 31;120(5):e2220578120. [Content Brief]
[8]. Li Y, et al. Structure of human Na(V)1.6 channel reveals Na(+) selectivity and pore blockade by 4,9-anhydro-tetrodotoxin. Nat Commun. 2023 Feb 23;14(1):1030. [Content Brief]