Sodium Channel, Nonvoltage-Gated 1, beta Proteins (SCNN1B)

Human Sodium Channel, Nonvoltage-Gated 1, beta (SCNN1B) interaction partners

1. SCNN1B was not associated with Salt Sensitivity of Blood Pressure in rare variant analyses.

2. Proteolytic cleavage activates epithelial sodium channel (SCNN) by removal of specific segments in finger domains of alpha and gamma subunits. Data suggest that the lower "palm" domain of SCNN1A is essential for allosteric activation of the SCNN heterotetramer [SCNN1A(1)-SCNN1B-SCNN1A(2)-SCNN1G].

3. In the present study, the SCNN1G gene was associated with 24-h urinary sodium excretion but was not related to blood pressure. The SCNN1A and SCNN1B genes were not associated with blood pressure either.

4. No association was found between single nucleotide polymorphism rs12447134 of sodium channel, nonvoltage-gated 1, beta protein (SCNN1B) gene with the onset of disease hypertension.

5. The Epithelial Sodium Channel Is a Modifier of the Long-Term Nonprogressive Phenotype Associated with F508del CFTR Mutations

6. The derlin-1 pathway therefore may represent a significant early checkpoint in the recognition and degradation of ENaC in mammalian cells.

7. 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.

8. deltabetagamma-ENaC is inhibited by CFTR but activated by cyclic AMP.

9. 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.

10. These results indicated a significant association between EH and SCNN1B methylation, which was affected by age, gender and antihypertensive therapy.

11. Three nonsynonymous amino acid variants in SCNN1B in nonwhite Cystic fibrosis patients with non-diagnostic CFTR genotypes was

12. These results do not suggest an important role for the T594M variant of the ENaC gene contributing to either the development or severity of hypertension in subjects of Indo-Aryan ancestry.

13. The transcriptional expression of alpha, beta, and gamma subunits of ENaC was elevated in nasal polyp compared to nasal mucosa

14. 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].

15. analysis of a novel frameshift mutation in the betaENaC gene in an isolated case of Liddle syndrome

16. Suggest that SCNN1B gene has important roles in blood pressure regulation in the Han Chinese population.

17. significant association between the rs3743966 SNP in intron 12 of epithelial sodium channel beta-subunit and essential hypertension

18. Suggest that beta-ENaC mediates cytotrophoblast migration and increasing beta-ENaC expression by HO-1 induction enhances migration.

19. ENaCbeta but not ENaCalpha expression is significantly lower in severe preeclampsia compared with normal pregnancy.

20. WNK4 inhibits ENaC channel activity independently of Nedd4-2-mediated ENaC ubiquitination.

Mouse (Murine) Sodium Channel, Nonvoltage-Gated 1, beta (SCNN1B) interaction partners

1. Apical fluid shear stress specifically downregulates beta-ENaC and gamma-ENaC subunits at the transcriptional level through an unidentified heat-insensitive paracrine basolateral factor in collecting duct principal cells.

2. Casein kinase 2 phosphorylation is an important regulator of ENaC activity and sodium handling by the aldosterone sensitive distal nephron.

3. N-linked glycans on each subunit are required for proper folding, maturation, surface expression, and function of the epithelial sodium channel.

4. Scnn1b-Tg mice exhibited an approximately 50% reduction mucociliary clearance

5. Loss of betaENaC function resulted in meibomian gland disease and severe ocular surface damage that phenocopied aspects of human pseudohypoaldosteronism-1 MG disease and was sex dependent.

6. The derlin-1 pathway therefore may represent a significant early checkpoint in the recognition and degradation of ENaC in mammalian cells.

7. Nedd4-2-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.

8. Data indicate that insulin receptor (InsR) is important for epithelial sodium channel (ENaC) activity.

9. Our findings are consistent with the role of betaENaC as a vascular smooth muscle cell mechanosensor and function of evolutionarily related nematode degenerin proteins.

10. These data suggest that adenylyl cyclase VI mediates vasopressin-stimulated ENaC activity in the kidney.

11. Cys substitutions at sites in the wrist domains of the beta and gamma subunits alter the Na+ self-inhibition response.

12. ENaC 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.

13. These findings demonstrate that myogenic constriction in afferent arterioles is dependent on normal expression of betaENaC

14. loss of beta-ENaC associated with early signs of renal injury and increased mean arterial pressure

15. generation of transgenic mice with airway-specific overexpression of the epithelial Na(+) channel (ENaC) is an alternative approach to mimic cystic fibrosis ion transport pathophysiology in the lung

16. Airway surface liquid volume regulation determines different airway phenotypes in liddle compared with betaENaC-overexpressing mice.

17. Il-6 activates ENaC-beta channels in cortical collecting duct cells.

18. Dot1a and AF9 downregulate Na(+) transport, most likely by regulating ENaC mRNA and subsequent protein expression and ENaC activity.

19. Beta-ENaC is an important mediator of renal myogenic constriction-mediated renal blood flow autoregulation in vivo.

20. pore regions from the three ENaC subunits have an asymmetric organization