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Anti-Nav1.7 Mouse Antibody [P22E18]

Catalog No.: F3300

Application: Reactivity: Mouse

Usage Information

Dilution
IHC1:200-1:1000

Application
IHC

Reactivity
Mouse

Source
Mouse

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Positive Control	Mouse back skin
Negative Control

Datasheet & SDS

Biological Description

Specificity
Nav1.7 Mouse mAb detects endogenous levels of total Nav1.7 protein.

Clone
P22E18

Synonym(s)
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

Background
NaV1.7 is a voltage-gated sodium channel encoded by the SCN9A gene and is predominantly expressed in peripheral sensory neurons, including small-diameter nociceptive dorsal root ganglion (DRG) neurons, trigeminal ganglion neurons, and sympathetic neurons. Structurally, NaV1.7 consists of a large α-subunit forming the ion-conducting pore, organized into four homologous domains (DI–DIV), each containing six transmembrane segments (S1–S6), with voltage-sensing regions (S4) and a selectivity filter that confers sodium specificity; it may also associate with β-subunits that modulate gating and expression. Functionally, NaV1.7 plays a crucial role in amplifying small, slow depolarizations near resting membrane potential and setting the threshold for action potential initiation, acting as a “threshold channel” in pain-sensing neurons. Gain-of-function mutations in SCN9A cause hyperexcitability of nociceptors, leading to inherited pain syndromes such as inherited erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD), whereas loss-of-function mutations result in congenital insensitivity to pain. Through its low-threshold activation and slow inactivation kinetics, NaV1.7 tightly regulates neuronal excitability and is a major pharmacological target for pain therapeutics.

Background

NaV1.7 is a voltage-gated sodium channel encoded by the SCN9A gene and is predominantly expressed in peripheral sensory neurons, including small-diameter nociceptive dorsal root ganglion (DRG) neurons, trigeminal ganglion neurons, and sympathetic neurons. Structurally, NaV1.7 consists of a large α-subunit forming the ion-conducting pore, organized into four homologous domains (DI–DIV), each containing six transmembrane segments (S1–S6), with voltage-sensing regions (S4) and a selectivity filter that confers sodium specificity; it may also associate with β-subunits that modulate gating and expression. Functionally, NaV1.7 plays a crucial role in amplifying small, slow depolarizations near resting membrane potential and setting the threshold for action potential initiation, acting as a “threshold channel” in pain-sensing neurons. Gain-of-function mutations in SCN9A cause hyperexcitability of nociceptors, leading to inherited pain syndromes such as inherited erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD), whereas loss-of-function mutations result in congenital insensitivity to pain. Through its low-threshold activation and slow inactivation kinetics, NaV1.7 tightly regulates neuronal excitability and is a major pharmacological target for pain therapeutics.

References
https://pubmed.ncbi.nlm.nih.gov/39378238/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%