Na+ Channel Protein antibody
Quick Overview for Na+ Channel Protein antibody (ABIN271819)
Target
Reactivity
Host
Clonality
Conjugate
Application
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Cross-Reactivity (Details)
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Species reactivity (expected):Mouse and Rat.
Species reactivity (tested):Human. -
Purification
- Affinity Chromatography using epitope-specific immunogen.
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Application Notes
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ELISA: 1/20000approx. 1/40000. Western Blot: 1/500approx. 1/1000. Immunohistochemistry: 1/50approx. 1/200. Immunofluorescence: 1/50approx. 1/200.
Other applications not tested.
Optimal dilutions are dependent on conditions and should be determined by the user. -
Restrictions
- For Research Use only
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Concentration
- 1.0 mg/mL
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Buffer
- Phosphate buffered saline (PBS), pH ~7.2, 0.05 % Sodium Azide
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Preservative
- Sodium azide
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Precaution of Use
- This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
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Handling Advice
- Avoid repeated freezing and thawing.
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Storage
- 4 °C/-20 °C
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Storage Comment
- Store the antibody undiluted at 2-8 °C for one month or (in aliquots) at -20 °C for longer.
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- Na+ Channel Protein
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Background
- 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 (Liddel's syndrome) and loss-of-function mutations in alpha- or beta-ENaC causes pseudohypoaldosteronism (PHA-1).Synonyms: Sodium channel protein brain pan, Sodium channel protein pan, Voltage-gated sodium channe pan
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Molecular Weight
- approx. 230 kDa
Target
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