Nav1.7 Antibody
(Synonyms: NENA, SCN9A, Sodium channel protein type 9 subunit alpha, Neuroendocrine sodium channel, Peripheral sodium channel 1, Sodium channel protein type IX subunit alpha, Voltage-gated sodium channel subunit alpha Nav1.7, hNE-Na, PN1)Nav1.7 Antibody is a Rabbit-derived and non-conjugated IgG Polyclonal antibody, targeting to Nav1.7.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P
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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
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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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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|---|---|---|
| Dilution Ratio | 1:1000-2000 | 1:100-200 |
Product Details
Nav1.7 Antibody is a Rabbit-derived and non-conjugated IgG Polyclonal antibody, targeting to Nav1.7.
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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 Nav1.7.
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
Nav1.7 is a Pore-forming subunit of Nav1.7, a voltage-gated sodium (Nav) channel that directly mediates the depolarizing phase of action potentials in excitable membranes. Navs, also called VGSCs (voltage-gated sodium channels) or VDSCs (voltage-dependent sodium channels), operate by switching between closed and open conformations depending on the voltage difference across the membrane. In the open conformation they allow Na(+) ions to selectively pass through the pore, along their electrochemical gradient. The influx of Na(+) ions provokes membrane depolarization, initiating the propagation of electrical signals throughout cells and tissues. Nav1.7 plays a crucial role in controlling the excitability and action potential propagation from nociceptor neurons, thereby contributing to the sensory perception of pain[1][2][3][4][5][6][7][8][9][10][11].
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Subcellular Localization
Cell membrane; Cell projection, neuron projection; Cell projection, axon
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Expression
Tissue_Specificity: Expressed strongly in dorsal root ganglion, with only minor levels elsewhere in the body, smooth muscle cells, MTC cell line and C-cell carcinoma. Also expressed in vagus nerves within the head and neck region. Isoform 1 is expressed preferentially in the central and peripheral nervous system. Isoform 2 is expressed preferentially in the dorsal root ganglion. -
Isoforms & Post-Translational Modification
Nav1.
Phosphorylation at Ser-1490 by PKC in a highly conserved cytoplasmic loop increases peak sodium currents. -
Subunit
The Nav1.7 voltage-gated sodium channel consists of an ion-conducting alpha subunit SCN9A 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.
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SwissProt ID
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Synonyms
NENA, SCN9A, Sodium channel protein type 9 subunit alpha, Neuroendocrine sodium channel, Peripheral sodium channel 1, Sodium channel protein type IX subunit alpha, Voltage-gated sodium channel subunit alpha Nav1.7, hNE-Na, PN1
Documentation
References
[1]. Li Z, et al. Dissection of the structure-function relationship of Na(v) channels. Proc Natl Acad Sci U S A. 2024 Feb 27;121(9):e2322899121. [Content Brief]
[2]. Wu T, et al. Critical role of extracellular loops in differential modulations of TTX-sensitive and TTX-resistant Na(v) channels. Proc Natl Acad Sci U S A. 2025 Aug 12;122(32):e2510355122. [Content Brief]
[3]. Cummins TR, et al. Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy. J Neurosci. 2004 Sep 22;24(38):8232-6. [Content Brief]
[4]. Choi JS, et al. Inherited erythermalgia: limb pain from an S4 charge-neutral Na channelopathy. Neurology. 2006 Nov 14;67(9):1563-7. [Content Brief]
[5]. Fertleman CR, et al. SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes. Neuron. 2006 Dec 7;52(5):767-74. [Content Brief]
[6]. Cox JJ, et al. An SCN9A channelopathy causes congenital inability to experience pain. Nature. 2006 Dec 14;444(7121):894-8. [Content Brief]
[7]. Han C, et al. Early- and late-onset inherited erythromelalgia: genotype-phenotype correlation. Brain. 2009 Jul;132(Pt 7):1711-22. [Content Brief]
[8]. Eberhardt M, et al. Inherited pain: sodium channel Nav1.7 A1632T mutation causes erythromelalgia due to a shift of fast inactivation. J Biol Chem. 2014 Jan 24;289(4):1971-80. [Content Brief]
[9]. Tan ZY, et al. Protein kinase C enhances human sodium channel hNav1.7 resurgent currents via a serine residue in the domain III-IV linker. FEBS Lett. 2014 Nov 3;588(21):3964-9. [Content Brief]
[10]. Ahuja S, et al. Structural basis of Nav1.7 inhibition by an isoform-selective small-molecule antagonist. Science. 2015 Dec 18;350(6267):aac5464. [Content Brief]
[11]. Klugbauer N, et al. Structure and functional expression of a new member of the tetrodotoxin-sensitive voltage-activated sodium channel family from human neuroendocrine cells. EMBO J. 1995 Mar 15;14(6):1084-90. [Content Brief]
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