Minireview: regulation of epithelial Na+ channel trafficking.

No abstract is available for this paper.

• Publication year

  2005

• Venue

  Endocrinology

• Publication date

  2005-12-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1210/EN.2005-0894PMID 16150899
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Neutrophil elastase activates near-silent epithelial Na+ channels and increases airway epithelial Na+ transport.

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• 14-3-3 Proteins Modulate the Expression of Epithelial Na+ Channels by Phosphorylation-dependent Interaction with Nedd4-2 Ubiquitin Ligase*

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• Nedd4-2 Phosphorylation Induces Serum and Glucocorticoid-regulated Kinase (SGK) Ubiquitination and Degradation*

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• Overexpression of the epithelial Na+ channel gamma subunit in collecting duct cells: interactions of Liddle's mutations and steroids on expression and function.

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• Ikappab kinase-beta (ikkbeta) modulation of epithelial sodium channel activity.

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• ENaC subunit-subunit interactions and inhibition by syntaxin 1A.

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• Functional Polymorphism in the Carboxyl Terminus of the α-Subunit of the Human Epithelial Sodium Channel*

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• cAMP and Serum and Glucocorticoid-inducible Kinase (SGK) Regulate the Epithelial Na+ Channel through Convergent Phosphorylation of Nedd4-2*

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• Relative Contribution of Nedd4 and Nedd4-2 to ENaC Regulation in Epithelia Determined by RNA Interference*

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• Distinct Pools of Epithelial Sodium Channels Are Expressed at the Plasma Membrane*

  2004influential reference
• Increased airway epithelial Na+ absorption produces cystic fibrosis-like lung disease in mice

  2004cited by this paper
• A naturally occurring human Nedd4-2 variant displays impaired ENaC regulation in Xenopus laevis oocytes.

  2004cited by this paper
• Fluorescence Resonance Energy Transfer Analysis of Subunit Stoichiometry of the Epithelial Na+ Channel*

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• Rho Small GTPases Activate the Epithelial Na+ Channel*

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• IκB Kinase-β (IKKβ) Modulation of Epithelial Sodium Channel Activity*

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• Syntaxin 1A Regulates ENaC Channel Activity*

  2004cited by this paper
• cAMP and SGK Regulate ENaC Through Convergent Phosphorylation of Nedd4-2

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• Epithelial Sodium Channels Are Activated by Furin-dependent Proteolysis*

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• Serine protease activation of near-silent epithelial Na+ channels.

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• Targeted degradation of ENaC in response to PKC activation of the ERK1/2 cascade.

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• Alternate promoters and variable splicing lead to hNedd4-2 isoforms with a C2 domain and varying number of WW domains.

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• Arachidonic Acid Regulates Surface Expression of Epithelial Sodium Channels*

  2003cited by this paper
• The role of individual Nedd4–2 (KIAA0439) WW domains in binding and regulating epithelial sodium channels

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• Syntaxin 1A Regulates ENaC via Domain-specific Interactions*

  2003cited by this paper
• cAMP Increases Density of ENaC Subunits in the Apical Membrane of MDCK Cells in Direct Proportion to Amiloride-sensitive Na+ Transport

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• Synergistic Activation of ENaC by Three Membrane-bound Channel-activating Serine Proteases (mCAP1, mCAP2, and mCAP3) and Serum- and Glucocorticoid-regulated Kinase (Sgk1) in Xenopus Oocytes

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• Interactions of beta and gamma ENaC with Nedd4 can be facilitated by an ERK-mediated phosphorylation.

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• Interactions of β and γENaC with Nedd4 Can Be Facilitated by an ERK-mediated Phosphorylation*

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• Salt and blood pressure: new insight from human genetic studies.

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• Abnormal regulation of ENaC: syndromes of salt retention and salt wasting by the collecting duct.

  2002influential reference
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• Serum and Glucocorticoid-regulated Kinase Modulates Nedd4-2-mediated Inhibition of the Epithelial Na+Channel*

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• Common variant of human NEDD4L activates a cryptic splice site to form a frameshifted transcript

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• Na Self Inhibition of Human Epithelial Na Channel

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• The transmembrane serine protease (TMPRSS3) mutated in deafness DFNB8/10 activates the epithelial sodium channel (ENaC) in vitro.

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• A single WW domain is the predominant mediator of the interaction between the human ubiquitin-protein ligase Nedd4 and the human epithelial sodium channel.

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• Solution structure of a Nedd4 WW domain–ENaC peptide complex

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• ENaC Degradation in A6 Cells by the Ubiquitin-Proteosome Proteolytic Pathway*

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• SGK integrates insulin and mineralocorticoid regulation of epithelial sodium transport.

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• Characterization of Interactions between Nedd4 and β and γENaC Using Surface Plasmon Resonance

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• Distinct characteristics of two human Nedd4 proteins with respect to epithelial Na(+) channel regulation.

  2001cited by this paper
• Aldosterone induces rapid apical translocation of ENaC in early portion of renal collecting system: possible role of SGK.

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• A novel mouse Nedd4 protein suppresses the activity of the epithelial Na+ channel

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• Characterization of interactions between Nedd4 and beta and gammaENaC using surface plasmon resonance.

  2001cited by this paper
• Multiple WW Domains, but Not the C2 Domain, Are Required for Inhibition of the Epithelial Na+ Channel by Human Nedd4*

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• Regulation of Receptor Fate by Ubiquitination of Activated β2-Adrenergic Receptor and β-Arrestin

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• Regulation of epithelial sodium channel activity through a region of the carboxyl terminus of the alpha -subunit. Evidence for intracellular kinase-mediated reactions.

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• Non-coordinate Regulation of Endogenous Epithelial Sodium Channel (ENaC) Subunit Expression at the Apical Membrane of A6 Cells in Response to Various Transporting Conditions*

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• Liddle's syndrome mutations disrupt cAMP-mediated translocation of the epithelial Na(+) channel to the cell surface.

  2000cited by this paper
• Human Nedd4 interacts with the human epithelial Na+ channel: WW3 but not WW1 binds to Na+-channel subunits.

  2000cited by this paper
• Regulation of the Amiloride-sensitive Epithelial Sodium Channel by Syntaxin 1A*

  1999cited by this paper
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  1999cited by this paper
• All Three WW Domains of Murine Nedd4 Are Involved in the Regulation of Epithelial Sodium Channels by Intracellular Na+ *

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  1999cited by this paper
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  1999cited by this paper
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  1999cited by this paper
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  1998cited by this paper
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• Electrophysiological and Biochemical Evidence That DEG/ENaC Cation Channels Are Composed of Nine Subunits*

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• The Activity of the Epithelial Sodium Channel Is Regulated by Clathrin-mediated Endocytosis*

  1997cited by this paper
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  1997cited by this paper
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• Amiloride-sensitive Na+ channels: Insights and outlooks

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• Identification of a PY motif in the epithelial Na channel subunits as a target sequence for mutations causing channel activation found in Liddle syndrome.

  1996cited by this paper
• Early death due to defective neonatal lung liquid clearance in αENaC-deficient mice

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• Liddle disease caused by a missense mutation of beta subunit of the epithelial sodium channel gene.

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• Cystic fibrosis airway epithelia fail to kill bacteria because of abnormal airway surface fluid.

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• Cell surface expression of the epithelial Na channel and a mutant causing Liddle syndrome: a quantitative approach.

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• Aldosterone-induced increase in the abundance of Na+ channel subunits.

  1996cited by this paper
• Early death due to defective neonatal lung liquid clearance in alpha-ENaC-deficient mice.

  1996cited by this paper
• WW domains of Nedd4 bind to the proline‐rich PY motifs in the epithelial Na+ channel deleted in Liddle's syndrome.

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