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Phospho-SCNN1B (Ser633) Polyclonal Antibody
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Product Details
OSS00145W-100UL
Applications
Tested Dilution
Publications
Product Specifications
Species Reactivity
Mouse,
Rat
Host/Isotype
Sheep
/ Ig
Class
Polyclonal
Type
Antibody
Immunogen
A synthetic peptide to phospho S633 of rat amiloride-sensitive sodium channel subunit beta (SCNN1B, SCNEB) conjugated to an immunogenic carrier protein was used as the immunogen
Conjugate
Form
Lyophilized
Concentration
Conc. 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 with the corresponding sequence in mouse.
Specificity of this antibody: SCNN1B.
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; Beta ENaC; Beta-ENaC; Beta-NaCH; ENaC beta; Epithelial Na(+) channel subunit beta; Epithelial sodium channel subunit beta; Nonvoltage-gated sodium channel 1 subunit beta; SCNEB; SCNN 1B; sodium channel, nonvoltage-gated 1, beta; sodium channel, nonvoltage-gated, type I, beta
Gene Aliases: RNENACB; Scnn1b
UniProt ID: (Mouse) Q9WU38, (Rat) P37090
Entrez Gene ID: (Mouse) 20277, (Rat) 24767
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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