Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Stimulation of the epithelial sodium channel (ENaC) by cAMP involves putative ERK phosphorylation sites in the C termini of the channel's beta- and gamma-subunit.

The Journal of biological chemistry - 14 Apr 2006

Yang Li-Min, Rinke Ralf, Korbmacher Christoph

Abstract excerpt

The mechanisms involved in the regulation of the epithelial sodium channel (ENaC) via the cAMP pathway are not yet completely understood. The aim of the present study was to investigate cAMP-mediated ENaC regulation in Xenopus laevis oocytes heterologously expressing the three subunits (alphabetagamma) of rat ENaC and to determine the ENaC regions important for mediating the stimulatory effect of cAMP. In oocytes...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to 1-Methyl-3-isobutylxanthine
Share to Colforsin

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Cyclic AMP-Dependent Protein Kinases

Share to Endosomal Sorting Complexes Required for Transport

Share to Epithelial Sodium Channels

Share to Nedd4 Ubiquitin Protein Ligases

Share to RNA, Complementary

Share to Xenopus Proteins

Source

Identifiers

PMID: 16476738
DOI: 10.1074/jbc.M512046200

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Stimulation of the epithelial sodium channel (ENaC) by cAMP involves putative ERK phosphorylation sites in the C termini of the channel's beta- and gamma-subunit.PMID 16476738Read ↗

The phosphorylation site T613 in the β-subunit of rat epithelial Na+ channel (ENaC) modulates channel inhibition by Nedd4-2.Semantic proximity Read ↗

Progesterone down-regulates the open probability of the amiloride-sensitive epithelial sodium channel via a Nedd4-2-dependent mechanism.Semantic proximity Read ↗

Proteolytic processing of the epithelial sodium channel gamma subunit has a dominant role in channel activation.Semantic proximity Read ↗

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

Regulatory interactions of N1303K-CFTR and ENaC in Xenopus oocytes: evidence that chloride transport is not necessary for inhibition of ENaC.Semantic proximity Read ↗

Activation of the Ae4 (Slc4a9) cation-driven Cl-/HCO3- exchanger by the cAMP-dependent protein kinase in salivary gland acinar cells.Semantic proximity Read ↗

Liddle-Mutation of the β-Subunit, but not the γ-Subunit, Attenuates Protein Kinase C-Mediated Inhibition of Human Epithelial Sodium Channels (hENaC).Semantic proximity Read ↗

Open probability of the epithelial sodium channel is regulated by intracellular sodium.Semantic proximity Read ↗

A mutation of the epithelial sodium channel associated with atypical cystic fibrosis increases channel open probability and reduces Na+ self inhibition.Semantic proximity Read ↗

Phosphorylation and modulation of hyperpolarization-activated HCN4 channels by protein kinase A in the mouse sinoatrial node.Semantic proximity Read ↗

A mutation in the β-subunit of ENaC identified in a patient with cystic fibrosis-like symptoms has a gain-of-function effect.Semantic proximity Read ↗

Cleavage in the {gamma}-subunit of the epithelial sodium channel (ENaC) plays an important role in the proteolytic activation of near-silent channels.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.