Thermo Fisher Scientific SCN11A Polyclonal Antibody

Applications

Tested Dilution

Publications

Western Blot (WB)

1:300-1:2,000

-

Immunohistochemistry (IHC)

1:300-1:2,000

-

Miscellaneous PubMed (Misc)

-

View 2 publications 2 publications

Product Specifications

Species Reactivity

Human

Published species

Not Applicable

Host/Isotype

Rabbit / Ig

Class

Polyclonal

Type

Antibody

Immunogen

A synthetic peptide from the internal region of human Sodium channel protein type 11 subunit alpha (SCN11A, Nav1.9) conjugated to an immunogenic carrier protein was used as the immunogen

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Lyophilized

Concentration

Conc. Not Determined

Storage buffer

whole serum

Contains

no preservative

Storage conditions

Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles. Glycerol (1:1) may be added for added stability.

Shipping conditions

Ambient (domestic); Wet ice (international)

Product Specific Information

Reconstitute in 100 µL of sterile water. Centrifuge to remove any insoluble material.

Specificity of this antibody: SCN11A.

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.