Evidence map›Paper›PMID 12460120›Full record

ReviewThe Biochemical journal2003

Regulation of the epithelial sodium channel by accessory proteins.

Kelly Gormley, Yanbin Dong, Giuseppe A Sagnella

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Aldosterone regulates microRNAs in the cortical collecting duct to alter sodium transport.Journal of the American Society of Nephrology : JASN · 2014
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Prostasin: a possible candidate gene for human hypertension.American journal of hypertension · 2008
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Kelly GormleyDivision of Neurosciences, St. George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK.
Yanbin Dong
Giuseppe A Sagnella
St George's, University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epithelial sodium channel (ENaC) is of fundamental importance in the control of sodium fluxes in epithelial cells. Modulation of sodium reabsorption through the distal nephron ENaC is an important component in the overall control of sodium balance, blood volume and thereby of blood pressure. This is clearly demonstrated by rare genetic disorders of sodium-channel activity (Liddle's syndrome and pseudohypoaldosteronism type 1), associated with contrasting effects on blood pressure. The mineralocorticoid aldosterone is a well-established modulator of sodium-channel activity. Considerable insight has now been gained into the intracellular signalling pathways linking aldosterone-mediated changes in gene transcription with changes in ion transport. Activating pathways include aldosterone-induced proteins and especially the serum- and glucocorticoid-inducible kinase (SGK) and the small G-protein, K-Ras 2A. Targeting of the ENaC for endocytosis and degradation is now emerging as a major mechanism for the down-regulation of channel activity. Several proteins acting in concert are an intrinsic part of this process but Nedd4 (neural precursor cell expressed developmentally down-regulated 4) is of central importance. Other mechanisms known to interact with ENaC and affect sodium transport include channel-activating protease 1 (CAP-1), a membrane-anchored protein, and the cystic fibrosis transmembrane regulator. The implications of research on accessory factors controlling ENaC activity are wide-ranging. Understanding cellular mechanisms controlling ENaC activity may provide a more detailed insight not only of ion-channel abnormalities in cystic fibrosis but also of the link between abnormal renal sodium transport and essential hypertension.

Indexed as

Nuclear ProteinsUbiquitin-Protein LigasesAmino Acid SequenceAnimalsCalcium-Binding ProteinsClathrinEndocytosisEndosomal Sorting Complexes Required for TransportEpithelial Sodium ChannelsHumansHypertensionImmediate-Early ProteinsKidney DiseasesLigasesMineralocorticoidsMolecular Sequence DataCalcium-Binding ProteinsClathrinEndosomal Sorting Complexes Required for TransportEpithelial Sodium ChannelsImmediate-Early ProteinsLigasesMineralocorticoidsNedd4 protein, humanNedd4 Ubiquitin Protein LigasesNuclear ProteinsProteinsProtein Serine-Threonine KinasesSerum-Glucocorticoid Regulated KinasesSodium ChannelsUbiquitinUbiquitin-Protein Ligases

Identifiers

PMID12460120
PMCPMC1223251
OpenAlexW2065844414

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.