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QED Bioscience
Nav1.7 Na+ Channel Monoclonal Antibody (S68-6)
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FIGURE: 1 / 5
Nav1.7 Na+ Channel Antibody (11517-100UG) in ICC/IF
Immunocytochemistry/Immunofluorescence analysis using Mouse Anti-Nav1.7 Monoclonal Antibody, Clone N68/6 (11517). Tissue: Neuroblastoma cells (SH-SY5Y). Species: Human. Fixation: 4% PFA for 15 min. Primary Antibody: Mouse Anti-Nav1.7 Monoclonal Antibody (11517) at 1:100 for overnight at 4°C with slow rocking. Secondary Antibody: AlexaFluor 488 at 1:1000 for 1 hour at RT. Counterstain: Phalloidin-iFluor 647 ... View More
Product Details
11517-100UG
Applications
Tested Dilution
Publications
Product Specifications
Species Reactivity
Human,
Mouse,
Rat
Host/Isotype
Mouse
/ IgG1
Class
Monoclonal
Type
Antibody
Clone
S68-6
Immunogen
Fusion protein, aa 1751-1946 (cytoplasmic C-terminus) of human Nav1.7 (accession no. Q15858).
Conjugate
Form
Liquid
Concentration
0.5-1.0 mg/mL
Purification
Protein A
Storage buffer
PBS, pH 7.4, with 50% glycerol
Contains
0.09% sodium azide
Storage conditions
-20°C, Avoid Freeze/Thaw Cycles
Shipping conditions
Ambient (domestic); Wet ice (international)
Target Information
Epithelial sodium channels are amiloride-sensitive members of the Degenerin/epithelial sodium channel (Deg/ENaC) superfamily of ion channels. Members of this superfamily of ion channels share organizational similarity in that they all possess two short intracellular amino and carboxyl termini, two short membrane spanning segments, and a large extracellular loop with a conserved cysteine-rich region. There are three homologous isoforms of the ENaC (alpha, beta, and gamma) protein. ENaC in the kidney, lung, and colon plays an essential role in trans-epithelial sodium and fluid balance. ENaC also mediates aldosterone-dependent sodium reabsorption in the distal nephron of the kidney, thus regulating blood pressure. ENaC is thought to be regulated, in part, through association with the cystic fibrosis transmembrane conductance regulator (CFTR) chloride ion channel. Gain-of-function mutations in beta- or gamma-ENaC can cause severe arterial hypertension (Liddels syndrome) and loss-of-function mutations in alpha- or beta-ENaC causes pseudohypoaldosteronism (PHA-1).
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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Bioinformatics
Protein Aliases: hNaN; hNE Na; hNE-Na; KIAA1356; MED; NAC1; NAC2; NAC3; Nav1.1; Nav1.2; Nav1.3; Nav1.4; Nav1.5; Nav1.6; Nav1.8; Nav1.9; NE; NE NA; Neuroendocrine sodium channel; Peripheral sodium channel 1; PN1; SCN1; SCN10A; SCN11A; SCN12A; SCN1A; SCN2A1; SCN2A2; SCN3A; SCN4A; SCN5A; SCN8A; SNS2; sodium channel 25; Sodium channel protein type 9 subunit alpha; Sodium channel protein type IX subunit alpha; sodium channel, voltage gated, type IX alpha subunit; sodium channel, voltage-gated, type 9, alpha polypeptide; sodium channel, voltage-gated, type IX, alpha polypeptide; sodium channel, voltage-gated, type IX, alpha subunit; voltage-gated sodium channel alpha subunit Nav1.7; Voltage-gated sodium channel subunit alpha Nav1.7
Gene Aliases: ETHA; FEB3B; GEFSP7; HSAN2D; Kiaa4197; mKIAA4197; Nav1.7; NE-NA; NENA; PN1; Scn2a; SCN9A; SFNP
UniProt ID: (Human) Q15858, (Mouse) Q62205, (Rat) O08562
Entrez Gene ID: (Human) 6335, (Mouse) 20274, (Rat) 78956
sodium ion transport
inflammatory response
response to toxic substance
post-embryonic development
neuronal action potential
sensory perception of pain
regulation of ion transmembrane transport
sodium ion transmembrane transport
behavioral response to pain
regulation of postsynaptic membrane potential
membrane depolarization during action potential
transport
ion transport
transmembrane transport
rhythmic excitation
Performance Guarantee
If an Invitrogen™ antibody doesn't perform as described on our website or datasheet,we'll replace the product at no cost to you, or provide you with a credit for a future purchase.*
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