missing translation for 'onlineSavingsMsg'
Learn More

Invitrogen™ SCN9A Biosimilar Recombinant Monoclonal Antibody
GREENER_CHOICE

Recombinant Monoclonal Antibody

£397.00 - £1002.00

Specifications

Antigen SCN9A Biosimilar
Concentration 1 mg/mL
Content And Storage -20°C, Avoid Freeze/Thaw Cycles
Applications ELISA, Flow Cytometry, Functional Assay, Surface Plasmon Resonance
Classification Recombinant Monoclonal
View More Specs

Products 2
Product Code Brand Quantity Price Quantity & Availability  
Product Code Brand Quantity Price Quantity & Availability  
30284269
GREENER_CHOICE
View Documents
Invitrogen™
MA558939
100 μg
£397.00
100µg
View alternative products
Save Up to 
»
Please to purchase this item. Need a web account? Register with us today!
30282977
View Documents
Invitrogen™
MA558940
1 mg
£1002.00
1mg
View alternative products
Save Up to 
»
Please to purchase this item. Need a web account? Register with us today!
Description

Description

For reconstitution, add sterile, distilled water to achieve a final antibody concentration of 1 mg/mL. Gently shake to solubilize the protein completely. Do not vortex. Reconstituted products should be stored at -80 °. This antibody can also be cross referenced by the term Duke anti-NAv1.7.

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).
Specifications

Specifications

SCN9A Biosimilar
-20°C, Avoid Freeze/Thaw Cycles
Recombinant Monoclonal
Lyophilized
IgG1
Human
Primary
Protein A
1 mg/mL
ELISA, Flow Cytometry, Functional Assay, Surface Plasmon Resonance
Unconjugated
Human
RUO
25mM histidine with 8% sucrose, 0.01% Tween 80 and no preservative; pH 6.2
Antibody
Videos
SDS
Documents

Documents

Product Certifications
Product Content Correction

Your input is important to us. Please complete this form to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Thank You! Your feedback has been submitted. Fisher Scientific is always working to improve our content for you. We appreciate your feedback.