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Invitrogen
SCNN1B Monoclonal Antibody (7B8), PerCP
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Product Details
MA5-45354
Applications
Tested Dilution
Publications
Product Specifications
Species Reactivity
Mouse
Host/Isotype
Mouse
/ IgG1
Class
Monoclonal
Type
Antibody
Clone
7B8
Immunogen
Synthetic peptide from the C-terminal of Rat ENaC beta (aa. 617-638)
Conjugate
PerCP
PerCP
PerCP
Excitation/Emission Max
482/675 nm
View spectra
Form
Liquid
Concentration
1 mg/mL
Amount
100 µg
Purification
Protein G
Storage buffer
95.64mM phosphate/2.48mM MES, pH 7.4, with 0.5M EDTA
Contains
no preservative
Storage conditions
4°C
Shipping conditions
Ambient (domestic); Wet ice (international)
RRID
Product Specific Information
A 1:1,000 dilution of MA5-45354 was sufficient for detection of ENaC beta in 15 µg of Mouse whole kidney lysate by ECL immunoblot analysis using goat anti-mouse IgG:HRP as the secondary antibody.|Detects approximately 87kDa.
Target Information
Sodium permeable non-voltage-sensitive ion channel inhibited by the diuretic amiloride. Mediates the electrodiffusion of the luminal sodium (and water, which follows osmotically) through the apical membrane of epithelial cells. Controls the reabsorption of sodium in kidney, colon, lung and sweat glands. Also plays a role in taste perception. Heterotetramer of two alpha, one beta and one gamma subunit. A delta subunit can replace the alpha subunit. Interacts with the WW domains of NEDD4, NEDD4L, WWP1 and WWP2. Defects in SCNN1B are a cause of autosomal recessive pseudohypoaldosteronism type 1 (PHA1) [MIM:264350]. PHA1 is a rare salt wasting disease resulting from target organ unresponsiveness to mineralocorticoids. There are 2 forms of PHA1: the autosomal recessive form that is severe, and the dominant form which is more milder and due to defects in mineralocorticoid receptor. Autosomal recessive PHA1 is characterized by an often fulminant presentation in the neonatal period with dehydration, hyponatraemia, hyperkalaemia, metabolic acidosis, failure to thrive and weight loss. Defects in SCNN1B are a cause of Liddle syndrome. It is an autosomal dominant disorder characterized by pseudoaldosteronism and hypertension associated with hypokalemic alkalosis. The disease is caused by constitutive activation of the renal epithelial sodium channel.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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Bioinformatics
Protein Aliases: amiloride-sensitive sodium channel subunit beta; Beta ENaC; beta-ENaC; beta-NaCH; ENaC beta; epithelial Na(+) channel subunit beta; nonvoltage-gated sodium channel 1 subunit beta; SCNEB; SCNN 1B; unnamed protein product
UniProt ID: (Mouse) Q9WU38
Entrez Gene ID: (Mouse) 20277
regulation of sodium ion transport
neutrophil activation involved in immune response
renal system process
sodium ion transport
cellular sodium ion homeostasis
regulation of blood pressure
response to xenobiotic stimulus
gene expression
artery smooth muscle contraction
response to food
aldosterone metabolic process
erythrocyte homeostasis
multicellular organism growth
wound healing, spreading of epidermal cells
sodium ion transmembrane transport
epithelial fluid transport
multicellular organismal water homeostasis
sensory perception of salty taste
sensory perception of sour taste
potassium ion homeostasis
sodium ion homeostasis
mucus secretion
neutrophil mediated killing of bacterium
cellular response to acidic pH
sodium ion import across plasma membrane
cellular response to aldosterone
cellular response to vasopressin
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Performance Guarantee
If an Invitrogen™ antibody doesn't perform as described on our website or datasheet,we'll replace the product at no cost to you, or provide you with a credit for a future purchase.*
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