Product Description

ENaC β (phospho Thr615) Rabbit Polyclonal Antibody

Sizes: 50μL, 100μL

Catalogue Numbers: ES7125-50, ES7125-100

Lead times: 1-2 weeks, if manufacturer has product in stock

Manufacturer/Ship Location: China

Background: Nonvoltage-gated, amiloride-sensitive, sodium channels control fluid and electrolyte transport across epithelia in many organs. These channels are heteromeric complexes consisting of 3 subunits: alpha, beta, and gamma. This gene encodes the beta subunit, and mutations in this gene have been associated with pseudohypoaldosteronism type 1 (PHA1), and Liddle syndrome. [provided by RefSeq, Apr 2009],

Reactivity: Human, Mouse, Rat

Host: Rabbit

Applications: WB, IHC, IF, ELISA

Alternate Names: SCNN1B, Amiloride-sensitive sodium channel subunit beta, Beta-NaCH, Epithelial Na(+) channel subunit beta, Beta-ENaC, ENaCB, Nonvoltage-gated sodium channel 1 subunit beta, SCNEB

Clonality: Polyclonal

Immunogen: The antiserum was produced against synthesized peptide derived from human Nonvoltage-gated Sodium Channel 1 around the phosphorylation site of Thr615. AA range:581-630

Isotype: IgG

Target: ENaC β

Specificity: Phospho-ENaC β (T615) Polyclonal Antibody detects endogenous levels of ENaC β protein only when phosphorylated at T615.

Dilution: Western Blot: 1/500 - 1/2000. Immunohistochemistry: 1/100 - 1/300. Immunofluorescence: 1/200 - 1/1000. ELISA: 1/10000. Not yet tested in other applications.

Purification: The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

Concentration: 1 mg/ml,

Formlation: Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

Expression: Detected in placenta, lung and kidney (PubMed:7762608), Expressed in kidney (at protein level) (PubMed:22207244),

Observed Band (KD): 68kD

Fields: Taste transduction, Aldosterone-regulated sodium reabsorption

Function: Disease: 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
Disease: Defects in SCNN1B are a cause of Liddle syndrome [MIM: 177200]. 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
Function: Sodium permeable

Subcellular Location: Apical cell membrane, Multi-pass membrane protein Cytoplasmic vesicle membrane Apical membrane of epithelial cells

Storage and Stability: -20°C/1 year

Gene Name: SCNN1B

Protein Name: Amiloride-sensitive sodium channel subunit beta

Mouse Gene ID: 20277

Mouse SwissProt Number: Q9WU38

Rat Gene ID: 24767

Rat SwissProt Number: P37090

Research Use Only