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Nonvoltage-gated, amiloride-sensitive, sodium channels control fluid and electrolyte transport across epithelia in many organs. Additionally we are shipping SCNN1B Proteins (7) and SCNN1B Kits (4) and many more products for this protein.
Showing 10 out of 184 products:
Human Polyclonal SCNN1B Primary Antibody for WB - ABIN1881778
Song, Wei, Zhou, Lazrak, Liu, Londino, Squadrito, Matalon: Inhibition of lung fluid clearance and epithelial Na+ channels by chlorine, hypochlorous acid, and chloramines. in The Journal of biological chemistry 2010
Show all 3 Pubmed References
Human Polyclonal SCNN1B Primary Antibody for IF (p), IHC (p) - ABIN713471
Pasham, Pathare, Fajol, Rexhepaj, Michael, Pakladok, Alesutan, Rotte, Föller, Lang: OSR1-sensitive small intestinal Na+ transport. in American journal of physiology. Gastrointestinal and liver physiology 2012
The derlin-1 (show DERL1 Antibodies) pathway therefore may represent a significant early checkpoint in the recognition and degradation of ENaC (show SCNN1A Antibodies) in mammalian cells.
hENaC incorporating the Liddle-mutated beta-subunit lacks one or more PKC phosphorylation sites, thereby significantly reducing the inhibitory effect of PKC on Na(+) channel activity, whereas hENaC incorporating Liddle-mutated gamma-subunits remains as susceptible to PKC as wild-type hENaC.
deltabetagamma-ENaC (show SCNN1A Antibodies) is inhibited by CFTR (show CFTR Antibodies) but activated by cyclic AMP (show APRT Antibodies).
Results identify SCNN1B as a tumor-suppressive function that triggers UPR in gastric cancer cells, with implications for its potential clinical applications as a survival biomarker in gastric cancer patients.
These results indicated a significant association between EH and SCNN1B methylation, which was affected by age, gender and antihypertensive therapy.
Three nonsynonymous amino acid variants in SCNN1B in nonwhite Cystic fibrosis (show S100A8 Antibodies) patients with non-diagnostic CFTR (show CFTR Antibodies) genotypes was
These results do not suggest an important role for the T594M variant of the ENaC (show SCNN1A Antibodies) gene contributing to either the development or severity of hypertension in subjects of Indo (show IDO1 Antibodies)-Aryan ancestry.
The transcriptional expression of alpha, beta, and gamma subunits of ENaC (show SCNN1A Antibodies) was elevated in nasal polyp compared to nasal mucosa
causative mutation for Liddle's syndrome (LS) in this patient was identified to be a novel frameshift mutation. DNA sequencing resulted in exon 13 of SCNN1B gene: SCNN1B NM_000336.2:c.1 724_1730dupGGCCCAC [p.Pro5 75Argfs*17].
analysis of a novel frameshift mutation in the betaENaC gene in an isolated case of Liddle syndrome
Nedd4-2 (show NEDD4L Antibodies)-mediated ubiquitination of beta-ENaC leading to endocytosis and degradation of apical Na(+) channels is a key feature of hypoxia-induced inhibition of transepithelial alveolar Na(+) transport.
Data indicate that insulin receptor (InsR (show INSR Antibodies)) is important for epithelial sodium channel (ENaC (show SCNN1A Antibodies)) activity.
Our findings are consistent with the role of betaENaC as a vascular smooth muscle cell mechanosensor and function of evolutionarily related nematode degenerin (show ACCN1 Antibodies) proteins.
These data suggest that adenylyl cyclase VI mediates vasopressin (show AVP Antibodies)-stimulated ENaC (show SCNN1A Antibodies) activity in the kidney.
Cys (show DNAJC5 Antibodies) substitutions at sites in the wrist domains of the beta and gamma subunits alter the Na+ self-inhibition response.
ENaC (show SCNN1A Antibodies) is not a passive passenger in regulated epithelial vesicle trafficking, but plays a role in establishing and maintaining the pool of vesicles that respond to cAMP stimulation.
These findings demonstrate that myogenic constriction in afferent arterioles is dependent on normal expression of betaENaC
loss of beta-ENaC associated with early signs of renal injury and increased mean arterial pressure
generation of transgenic mice with airway-specific overexpression of the epithelial Na(+) channel (ENaC (show SCNN1A Antibodies)) is an alternative approach to mimic cystic fibrosis (show S100A8 Antibodies) ion transport pathophysiology in the lung
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.
sodium channel, nonvoltage-gated 1, beta
, sodium channel, nonvoltage-gated 1, beta (Liddle syndrome)
, amiloride-sensitive sodium channel subunit beta
, amiloride-sensitive sodium channel subunit beta 1
, 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
, Amiloride-sensitive sodium channel subunit beta
, epithelial amiloride-sensitive sodium channel beta subunit
, epithelial sodium channel ENaC beta subunit
, epithelial sodium channel, beta subunit
, amiloride sensitive epithelial sodium ion channel beta subunit
, epithelium sodium channel beta subunit
, ENaC beta
, amiloride sensitive sodium channel beta1 subunit
, sodium channel, nonvoltage-gated, type I, beta