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Invitrogen
SCNN1B Polyclonal Antibody
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Product Details
PA5-76060
Applications
Tested Dilution
Publications
Product Specifications
Species Reactivity
Human,
Mouse
Published species
C. elegans
Host/Isotype
Rabbit
/ IgG
Class
Polyclonal
Type
Antibody
Immunogen
Recombinant full length Human SCNN1B.
Conjugate
Form
Liquid
Concentration
1 mg/mL
Purification
Antigen affinity chromatography
Storage buffer
PBS, pH 7.2, with 50% 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
Ambient (domestic); Wet ice (international)
RRID
Product Specific Information
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is > 95% (by SDS-PAGE).
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.
Bioinformatics
Protein Aliases: Amiloride-sensitive sodium channel subunit beta; amiloride-sensitive sodium channel subunit beta 1; Beta ENaC; Beta-ENaC; Beta-NaCH; ENaC beta; Epithelial Na(+) channel subunit beta; epithelial sodium channel beta-2 subunit; epithelial sodium channel beta-3 subunit; nasal epithelial sodium channel beta subunit; Nonvoltage-gated sodium channel 1 subunit beta; SCNEB; SCNN 1B; sodium channel, non voltage gated 1 beta subunit; sodium channel, non-voltage-gated 1, beta subunit; sodium channel, nonvoltage-gated 1, beta
Gene Aliases: BESC1; ENaCb; ENaCbeta; SCNEB; SCNN1B
UniProt ID: (Human) P51168, (Mouse) Q9WU38
Entrez Gene ID: (Human) 6338, (Mouse) 20277
response to hypoxia
regulation of sodium ion transport
sodium ion transport
excretion
ion transmembrane transport
wound healing, spreading of epidermal cells
sodium ion transmembrane transport
multicellular organismal water homeostasis
sensory perception of taste
sodium ion homeostasis
transport
ion transport
response to stimulus
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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