Activation of the epithelial Na+ channel (ENaC) requires CFTR Cl- channel function

Nature ◽  
10.1038/46297 ◽  
1999 ◽  
Vol 402 (6759) ◽  
pp. 301-304 ◽  
Author(s):  
M. M. Reddy ◽  
M. J. Light ◽  
P. M. Quinton
Keyword(s):  
Na Channel ◽  
Channel Function ◽  
Cl Channel ◽  
Epithelial Na Channel

scholarly journals Differentiation of Epithelial Na+Channel Function

2005 ◽  
Vol 280 (25) ◽  
pp. 24181-24187 ◽  
Author(s):  
Vadim Shlyonsky ◽  
Arnaud Goolaerts ◽  
Ronald Van Beneden ◽  
Sarah Sariban-Sohraby
Keyword(s):  
Na Channel ◽  
Channel Function ◽  
Epithelial Na Channel

Associated Proteins and Renal Epithelial Na + Channel Function

1996 ◽  
Vol 149 (2) ◽  
pp. 123-132 ◽  
Author(s):  
I.I. Ismailov ◽  
B.K. Berdiev ◽  
A.L. Bradford ◽  
M.S. Awayda ◽  
C.M. Fuller ◽  
...  
Keyword(s):  
Na Channel ◽  
Channel Function ◽  
Associated Proteins ◽  
Epithelial Na Channel

scholarly journals Differential Effects of Protein Kinase C on the Levels of Epithelial Na+Channel Subunit Proteins

2000 ◽  
Vol 275 (33) ◽  
pp. 25760-25765 ◽  
Author(s):  
James D. Stockand ◽  
Hui-Fang Bao ◽  
Julie Schenck ◽  
Bela Malik ◽  
Pam Middleton ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Na Channel ◽  
Differential Effects ◽  
Kinase C ◽  
Epithelial Na Channel

scholarly journals CRISPR/Cas9 Mediated Knock Down of δ-ENaC Blunted the TNF-Induced Activation of ENaC in A549 Cells

2021 ◽  
Vol 22 (4) ◽  
pp. 1858
Author(s):  
Waheed Shabbir ◽  
Nermina Topcagic ◽  
Mohammed Aufy ◽  
Murat Oz
Keyword(s):  
A549 Cells ◽  
Na Channel ◽  
Na Current ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Knock Down ◽  
Whole Cell Patch Clamp ◽  
Glycosylation Sites ◽  
Epithelial Na Channel

Tumor necrosis factor (TNF) is known to activate the epithelial Na+ channel (ENaC) in A549 cells. A549 cells are widely used model for ENaC research. The role of δ-ENaC subunit in TNF-induced activation has not been studied. In this study we hypothesized that δ-ENaC plays a major role in TNF-induced activation of ENaC channel in A549 cells which are widely used model for ENaC research. We used CRISPR/Cas 9 approach to knock down (KD) the δ-ENaC in A549 cells. Western blot and immunofluorescence assays were performed to analyze efficacy of δ-ENaC protein KD. Whole-cell patch clamp technique was used to analyze the TNF-induced activation of ENaC. Overexpression of wild type δ-ENaC in the δ-ENaC KD of A549 cells restored the TNF-induced activation of whole-cell Na+ current. Neither N-linked glycosylation sites nor carboxyl terminus domain of δ-ENaC was necessary for the TNF-induced activation of whole-cell Na+ current in δ-ENaC KD of A549 cells. Our data demonstrated that in A549 cells the δ-ENaC plays a major role in TNF-induced activation of ENaC.

scholarly journals Acute effects of aldosterone on the epithelial Na channel in rat kidney

2015 ◽  
Vol 308 (6) ◽  
pp. F572-F578 ◽  
Author(s):  
Gustavo Frindt ◽  
Lawrence G. Palmer
Keyword(s):  
Rat Kidney ◽  
Surface Protein ◽  
Early Response ◽  
Surface Expression ◽  
Na Channel ◽  
Channel Activity ◽  
Acute Effects ◽  
Chronic Stimulation ◽  
Epithelial Na Channels ◽  
Epithelial Na Channel

The acute effects of aldosterone administration on epithelial Na channels (ENaC) in rat kidney were examined using electrophysiology and immunodetection. Animals received a single injection of aldosterone (20 μg/kg body wt), which reduced Na excretion over the next 3 h. Channel activity was assessed in principal cells of cortical collecting ducts as amiloride-sensitive whole cell clamp current ( INa). INa averaged 100 pA/cell, 20–30% of that reported for the same preparation under conditions of chronic stimulation. INa was negligible in control animals that did not receive hormone. The acute physiological response correlated with changes in ENaC processing and trafficking. These effects included increases in the cleaved forms of α-ENaC and γ-ENaC, assessed by Western blot, and increases in the surface expression of β-ENaC and γ-ENaC measured after surface protein biotinylation. These changes were qualitatively and quantitatively similar to those of chronic stimulation. This suggests that altered trafficking to or from the apical membrane is an early response to the hormone and that later increases in channel activity require stimulation of channels residing at the surface.

scholarly journals Maturation of the Epithelial Na+ Channel Involves Proteolytic Processing of the α- and γ-Subunits

2003 ◽  
Vol 278 (39) ◽  
pp. 37073-37082 ◽  
Author(s):  
Rebecca P. Hughey ◽  
Gunhild M. Mueller ◽  
James B. Bruns ◽  
Carol L. Kinlough ◽  
Paul A. Poland ◽  
...  
Keyword(s):  
Proteolytic Processing ◽  
Na Channel ◽  
Epithelial Na Channel

The serine/threonine kinases SGK2 and SGK3 are potent stimulators of the epithelial Na+ channel α,β,γ-ENaC

2003 ◽  
Vol 445 (6) ◽  
pp. 693-696 ◽  
Author(s):  
B. Friedrich ◽  
Y. Feng ◽  
P. Cohen ◽  
T. Risler ◽  
A. Vandewalle ◽  
...  
Keyword(s):  
Na Channel ◽  
Threonine Kinases ◽  
Epithelial Na Channel
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