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

Phospho-ENaC β (T615) Polyclonal Antibody detects endogenous levels of ENaC β protein only when phosphorylated at T615.The name of modified sites may be influenced by many factors, such as species (the modified site was not originally found in human samples) and the change of protein sequence (the previous protein sequence is incomplete, and the protein sequence may be prolonged with the development of protein sequencing technology). When naming, we will use the "numbers" in historical reference to keep the sites consistent with the reports. The antibody binds to the following modification sequence (lowercase letters are modification sites):PGtPP

SCNN1B

Amiloride-sensitive sodium channel subunit beta

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

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],

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 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.,PTM:Phosphorylated on serine and threonine residues.,similarity:Belongs to the amiloride-sensitive sodium channel family.,subcellular location:Apical membrane of epithelial cells.,subunit: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.,

Apical cell membrane ; Multi-pass membrane protein . Cytoplasmic vesicle membrane . Apical membrane of epithelial cells. .

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

>>Taste transduction ;
>>Aldosterone-regulated sodium reabsorption