ArticleBiochimica et biophysica acta2011
Cpt-cAMP activates human epithelial sodium channels via relieving self-inhibition.
Article in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Epithelial NaComprehensive Physiology · 2024Review
- Accessibility of ENaC extracellular domain central core residues.The Journal of biological chemistry · 2022Article
- Plasmin improves blood-gas barrier function in oedematous lungs by cleaving epithelial sodium channels.British journal of pharmacology · 2020Article
- Article
- CPT-cGMP Is A New Ligand of Epithelial Sodium Channels.International journal of biological sciences · 2016Review
- Epithelial Sodium and Chloride Channels and Asthma.Chinese medical journal · 2015Review
- Prolactin stimulates sodium and chloride ion channels in A6 renal epithelial cells.American journal of physiology. Renal physiology · 2015Article
- Proteolytic regulation of epithelial sodium channels by urokinase plasminogen activator: cutting edge and cleavage sites.The Journal of biological chemistry · 2015Article
- Regulation of epithelial sodium channels in urokinase plasminogen activator deficiency.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Intravenous S-ketamine does not inhibit alveolar fluid clearance in a septic rat model.PloS one · 2014Article
- δ ENaC: a novel divergent amiloride-inhibitable sodium channel.American journal of physiology. Lung cellular and molecular physiology · 2012Review
- Probing the structural basis of Zn2+ regulation of the epithelial Na+ channel.The Journal of biological chemistry · 2012Article
- 8-(4-chlorophenylthio)-guanosine-3',5'-cyclic monophosphate-Na stimulates human alveolar fluid clearance by releasing external Na+ self-inhibition of epithelial Na+ channels.American journal of respiratory cell and molecular biology · 2011Article
- Ketamine inhibits lung fluid clearance through reducing alveolar sodium transport.Journal of biomedicine & biotechnology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
External Na(+) self-inhibition is an intrinsic feature of epithelial sodium channels (ENaC). Cpt-cAMP regulates heterologous guinea pig but not rat αβγ ENaC in a ligand-gated manner. We hypothesized that cpt-cAMP may eliminate the self-inhibition of human ENaC thereby open channels. Regulation of self-inhibition by this compound in oocytes was analyzed using the two-electrode voltage clamp and Ussing chamber setups. External cpt-cAMP stimulated human but not rat and murine αβγ ENaC in a dose- and external Na(+) concentration-dependent fashion. Intriguingly, cpt-cAMP activated human δβγ more potently than αβγ channels, suggesting that structural diversity in ectoloop between human α, δ, and those ENaC of other species determines the stimulating effects of cpt-cAMP. Cpt-cAMP increased the ratio of stationary and maximal currents. Mutants having abolished self-inhibition (β(ΔV348) and γ(H233R)) almost completely eliminated cpt-cAMP mediated activation of ENaC. On the other hand, mutants both enhancing self-inhibition and elevating cpt-cAMP sensitivity increased the stimulating effects of the compound. This compound, however, could not activate already fully opened channels, e.g., degenerin mutation (αβ(S520C)γ) and the proteolytically cleaved ENaC by plasmin. Cpt-cAMP activated native ENaC to the same extent as that for heterologous ENaC in human lung epithelial cells. Our data demonstrate that cpt-cAMP, a broadly used PKA activator, stimulates human αβγ and δβγ ENaC channels by relieving self-inhibition.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.