
Thermo Fisher Scientific SCN9A Monoclonal Antibody (5A11)
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Applications
Tested Dilution
Publications
Western Blot (WB)
1-5 µg/mL
ELISA (ELISA)
10 µg/mL
Product Specifications
Species Reactivity
Human, Rat
Host/Isotype
Mouse / IgG2b, kappa
Class
Monoclonal
Type
Antibody
Clone
5A11
Immunogen
SCN9A (NP_002968, 269 a.a. approximately 339 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. if (typeof window.$mangular === undefined
|| !window.$mangular) { window.$mangular = {}; } $mangular.antigenJson = \[{
targetFamily:
SCN9A,
uniProtId:
Q15858-1,
ncbiNodeId:
9606,
antigenRange:
269-339,
antigenLength:
1988,
antigenImageFileName:
H00006335-M01_SCN9A_Q15858-1_House_mouse.svg,
antigenImageFileNamePDP:
H00006335-M01_SCN9A_Q15858-1_House_mouse_PDP.jpeg,
sortOrder:
1}\]
; $mangular.isB2BCMGT = false
; $mangular.isEpitopesModalImageMultiSizeEnabled = true
;
View immunogen .st0{fill:#FFFFFF;} .st1{fill:#1E8AE7;}
Conjugate
Unconjugated Unconjugated Unconjugated
Form
Liquid
Concentration
See Label
Purification
Affinity chromatography
Storage buffer
PBS, pH 7.4
Contains
no preservative
Storage conditions
-20° C, Avoid Freeze/Thaw Cycles
Shipping conditions
Ambient (domestic); Wet ice (international)
Product Specific Information
Sequence of this protein is as follows: GNLKHKCFRN SLENNETLES IMNTLESEED FRKYFYYLEG SKDALLCGFS TDSGQCPEGY TCVKIGRNPD Y
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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