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Invitrogen
alpha-ENaC Monoclonal Antibody (14E10), FITC
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alpha-ENaC Antibody (MA5-45359) in IHC (P)
Immunohistochemistry analysis using Kidney. Fixation involved paraffin-embedded formalin-fixed treatment. Samples were incubated with ENaC alpha monoclonal antibody (Product # MA5-45359) at 1:100, followed by Goat Anti-Mouse ATTO 488 (green). Localization: Intercalated cells. Aquaporin 2 antibody staining in red.
Product Details
MA5-45359
Applications
Tested Dilution
Publications
Product Specifications
Species Reactivity
Mouse,
Rat
Host/Isotype
Mouse
/ IgG1
Class
Monoclonal
Type
Antibody
Clone
14E10
Immunogen
Synthetic peptide from the N-terminal of Rat ENaC alpha (aa. 46-68)
Conjugate
Excitation/Emission Max
498/517 nm
View spectra
Form
Liquid
Concentration
1 mg/mL
Purification
Protein G
Storage buffer
9.1mM sodium bicarbonate/PBS, pH 7.4, with 581mM DMSO, 123mM ethanolamine
Contains
no preservative
Storage conditions
4°C, store in dark
Shipping conditions
Ambient (domestic); Wet ice (international)
RRID
AB_2931813
Product Specific Information
A 1:1,000 dilution of MA5-45359 was sufficient for detection of ENaC alpha in 15 µg of Mouse whole kidney lysate by ECL immunoblot analysis using goat anti-mouse IgG:HRP as the secondary antibody.|Detects approximately 85kDa.
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 (Liddel’s 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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Bioinformatics
Protein Aliases: Alpha-ENaC; Alpha-NaCH; amiloride-sensitive epithelial sodium channel; Amiloride-sensitive sodium channel subunit alpha; ENaC alpha; epithelial Na(+) channel subunit alpha; epithelial sodium channel alpha subunit; Epithelial sodium channel subunit alpha; FLJ21883; Nonvoltage-gated sodium channel 1 subunit alpha; SCNEA; sodium channel, nonvoltage-gated 1 alpha; sodium channel, nonvoltage-gated, type I, alpha; sodium channel, nonvoltage-gated, type I, alpha polypeptide
Gene Aliases: ENaC; mENaC; RCNaCh; RCNaCh1; Renac; SCNEA; Scnn1; Scnn1a
UniProt ID: (Rat) P37089, (Mouse) Q61180
Entrez Gene ID: (Rat) 25122, (Mouse) 20276
Performance Guarantee
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