Thermo Fisher Scientific SCN1A Polyclonal Antibody
SCN1A 단백질을 인식하는 Thermo Fisher Scientific의 Rabbit Polyclonal Antibody. WB 및 IHC에 사용 가능하며, 인간·마우스·랫트 반응성. 동결건조 형태로 제공되며, 장기 보관 시 -20°C 권장. 연구용으로만 사용.
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Applications
| Application | Tested Dilution | Publications |
|---|---|---|
| Western Blot (WB) | 1:300–1:2,000 | - |
| Immunohistochemistry (IHC) | 1:300–1:2,000 | - |
| Miscellaneous PubMed (Misc) | - | View 2 publications |
Product Specifications
| 항목 | 내용 |
|---|---|
| Species Reactivity | Human, Mouse, Rat |
| Published Species | Not Applicable |
| Host / Isotype | Rabbit / Ig |
| Class | Polyclonal |
| Type | Antibody |
| Immunogen | A synthetic peptide from the C-terminal of Sodium channel protein type 1 subunit alpha (SCN1A, Nav1.1) conjugated to an immunogenic carrier protein |
| Conjugate | Unconjugated |
| Form | Lyophilized |
| Concentration | 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.
- The antigen is homologous in rat and human.
- Specificity of this antibody: SCN1A.
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 share organizational similarity with 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 plays an essential role in trans-epithelial sodium and fluid balance in the kidney, lung, and colon.
ENaC 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 (Liddell’s syndrome), and loss-of-function mutations in alpha- or beta-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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