
Thermo Fisher Scientific SCNN1G Polyclonal Antibody
Rabbit polyclonal antibody against human SCNN1G, validated for ICC/IF applications. Recognizes recombinant human SCNN1G with high specificity. Supplied as a liquid form, unconjugated, with antigen affinity purification. Suitable for research use only.
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Applications and Tested Dilution
| Application | Tested Dilution |
|---|---|
| Immunocytochemistry (ICC/IF) | 0.25–2 µg/mL |
Product Specifications
| 항목 | 내용 |
|---|---|
| Species Reactivity | Human |
| Host / Isotype | Rabbit / IgG |
| Class | Polyclonal |
| Type | Antibody |
| Immunogen | Recombinant Human SCNN1G. Recombinant protein control fragment (Product #RP-107801) |
| Conjugate | Unconjugated |
| Form | Liquid |
| Concentration | 0.05 mg/mL |
| Purification | Antigen affinity chromatography |
| Storage Buffer | PBS, pH 7.2, with 40% glycerol |
| Contains | 0.02% sodium azide |
| Storage Conditions | Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles. |
| Shipping Conditions | Wet ice |
| RRID | AB_2662930 |
Product Specific Information
- Immunogen sequence:
SEYGLQVILYI NEEEYNPFLV SSTGAKVIIH RQDEYPFVED VGTEIETAMV TSIGMHLTES FKLSEPYSQ - Ortholog identity: Highest antigen sequence identity to mouse (90%) and rat (90%).
Target Information
Epithelial sodium channels (ENaC) are amiloride-sensitive members of the degenerin/epithelial sodium channel (Deg/ENaC) superfamily of ion channels. Members of this superfamily share structural similarity, possessing 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 ENaC (α, β, and γ). ENaC in the kidney, lung, and colon plays an essential role in trans-epithelial sodium and fluid balance. It mediates aldosterone-dependent sodium reabsorption in the distal nephron, thereby regulating blood pressure. ENaC is also thought to be regulated through association with the CFTR chloride ion channel. Gain-of-function mutations in β- or γ-ENaC can cause severe arterial hypertension (Liddle’s syndrome), while loss-of-function mutations in α- or β-ENaC cause pseudohypoaldosteronism (PHA-1).
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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