Search
Bioss
SCNN1B Polyclonal Antibody
{{$productOrderCtrl.translations['antibody.pdp.commerceCard.promotion.promotions']}}
{{$productOrderCtrl.translations['antibody.pdp.commerceCard.promotion.viewpromo']}}
{{$productOrderCtrl.translations['antibody.pdp.commerceCard.promotion.promocode']}}: {{promo.promoCode}} {{promo.promoTitle}} {{promo.promoDescription}}. {{$productOrderCtrl.translations['antibody.pdp.commerceCard.promotion.learnmore']}}
Additional Information:
{{banner.description}}
Product Details
BS-4252R
Applications
Tested Dilution
Publications
Product Specifications
Species Reactivity
Human,
Mouse,
Rat
Host/Isotype
Rabbit
/ IgG
Class
Polyclonal
Type
Antibody
Immunogen
KLH conjugated synthetic peptide derived from human SCNN1B, amino acids 401-500.
Conjugate
Form
Liquid
Concentration
1 mg/mL
Purification
Protein A
Storage buffer
0.01M TBS, pH 7.4, with 1% BSA, 50% glycerol
Contains
0.02% ProClin 300
Storage conditions
-20°C
Shipping conditions
Ambient (domestic); Wet ice (international)
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.
References (0)
Have you cited this product in a publication?
Let us know so we can reference it here.
Bioinformatics
Protein Aliases: Amiloride-sensitive sodium channel subunit beta; amiloride-sensitive sodium channel subunit beta 1; Beta ENaC; Beta-ENaC; Beta-NaCH; ENaC beta; ENaC subunit beta; ENaC; sodium channel beta-2; Epithelial Na(+) channel subunit beta; epithelial sodium channel beta-2 subunit; epithelial sodium channel beta-3 subunit; Epithelial sodium channel subunit beta; mutant sodium channel epithelial 1 beta subunit; nasal ENaC; hnENac; nasal epithelial sodium channel beta subunit; Nonvoltage-gated sodium channel 1 subunit beta; SCNEB; SCNN 1B; sodium channel epithelial 1 beta subunit; sodium channel, non-voltage-gated 1, beta subunit; sodium channel, nonvoltage-gated 1, beta; sodium channel, nonvoltage-gated, type I, beta; unnamed protein product
Gene Aliases: BESC1; beta-ENaC; beta-NaCH; ENaCb; ENaCbeta; LIDLS1; PHA1B2; RNENACB; SCNEB; SCNN1B
UniProt ID: (Human) P51168, (Mouse) Q9WU38, (Rat) P37090
Entrez Gene ID: (Human) 6338, (Mouse) 20277, (Rat) 24767
leukocyte activation involved in inflammatory response
neutrophil activation involved in immune response
renal system process
ion transport
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
ion transmembrane transport
multicellular organism growth
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
regulation of sodium ion transport
transport
wound healing, spreading of epidermal cells
response to stimulus
sensory perception of taste
response to hypoxia
Disclaimer
Clicking the images or links will redirect you to a website hosted by BenchSci that provides third-party scientific content. Neither the content nor the BenchSci technology and processes for selection have been evaluated by us; we are providing them as-is and without warranty of any kind, including for use or application of the Thermo Fisher Scientific products presented.
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.*
Learn more
We're here to help
Get expert recommendations for common problems or connect directly with an on staff expert for technical assistance related to applications, equipment and general product use.
Contact tech support