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Invitrogen
Human SCNN1B (aa 333-476) Control Fragment Recombinant Protein
Product Details
RP-90439
Applications
Tested Dilution
Publications
Product Specifications
Species
Human
Expression System
E. coli
Amino acid sequence
GIYAMSGTETSIGVLVDKLQRMGEPYSPCTVNGSEVPVQNFYSDYNTTYSIQACLRSCFQDHMIRNCNCGHYLYPLPRGEKYCNNRDFPDWAHCYSDLQMSVAQRETCIGMCKESCNDTQYKMTISMADWPSEASEDWIFHVLS
Tag
His-ABP-tag
Class
Recombinant
Type
Protein
Purity
>80% by SDS-PAGE and Coomassie blue staining
Conjugate
Form
Liquid
Concentration
≥5.0 mg/mL
Purification
purified
Storage buffer
1M urea/PBS, pH 7.4
Contains
no preservative
Storage conditions
-20° C, Avoid Freeze/Thaw Cycles
Shipping conditions
Wet ice
Product Specific Information
Highest antigen sequence indentity to the following orthologs: Mouse (87%), Rat (87%).
This recombinant protein control fragment may be used for blocking experiments with the corresponding antibody, PA5-53342. In IHC/ICC and WB experiments, we recommend a 100x molar excess of the protein fragment control based on the concentration and the molecular weight. Pre-incubate the antibody-protein control fragment mixture for 30 min at room temperature.
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; amiloride-sensitive sodium channel subunit beta 1; Beta ENaC; Beta-ENaC; Beta-NaCH; 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) Q96KG2
Entrez Gene ID: (Human) 6338
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