Evidence map›Paper›PMID 10051674›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Epithelial sodium channel regulated by aldosterone-induced protein sgk.

S Y Chen, A Bhargava, L Mastroberardino, O C Meijer, J Wang, P Buse, G L Firestone, F Verrey, D Pearce

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed
17.4field-weighted citation impact, top 1% 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

218 citing papers in PubMed, 735 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Aldosterone-independent regulation of K + secretion in the distal nephron.Current opinion in nephrology and hypertension · 2024
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Renal tubular SGK1 is required to achieve blood pressure surge and circadian rhythm.American journal of physiology. Renal physiology · 2023
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

158 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 2 countries.

S Y ChenDivision of Nephrology, Departments of Medicine and Cellular and Molecular Pharmacology, Box 0532, University of California, San Francisco, CA 94143, USA.
A Bhargava
L Mastroberardino
O C Meijer
J Wang
P Buse
G L Firestone
F Verrey
D Pearce
University of California, Berkeley · USUniversity of Zurich · CHUniversity of California, San Francisco · US

Funding

MECHANISMS OF MINERALOCORTICOID RECEPTOR FUNCTIONR29DK051151 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI PEARCE, DAVID · 1996 to 2000
$100k
NIDDK NIH HHS R29 DK051151NIDDK NIH HHS R29-DK51151-03
6 · The paper itself

Abstract

Sodium homeostasis in terrestrial and freshwater vertebrates is controlled by the corticosteroid hormones, principally aldosterone, which stimulate electrogenic Na+ absorption in tight epithelia. Although aldosterone is known to increase apical membrane Na+ permeability in target cells through changes in gene transcription, the mechanistic basis of this effect remains poorly understood. The predominant early effect of aldosterone is to increase the activity of the epithelial sodium channel (ENaC), although ENaC mRNA and protein levels do not change initially. Rather, the open probability and/or number of channels in the apical membrane are greatly increased by unknown modulators. To identify hormone-stimulated gene products that modulate ENaC activity, a subtracted cDNA library was generated from A6 cells, a stable cell line of renal distal nephron origin, and the effect of candidates on ENaC activity was tested in a coexpression assay. We report here the identification of sgk (serum and glucocorticoid-regulated kinase), a member of the serine-threonine kinase family, as an aldosterone-induced regulator of ENaC activity. sgk mRNA and protein were strongly and rapidly hormone stimulated both in A6 cells and in rat kidney. Furthermore, sgk stimulated ENaC activity approximately 7-fold when they were coexpressed in Xenopus laevis oocytes. These data suggest that sgk plays a central role in aldosterone regulation of Na+ absorption and thus in the control of extracellular fluid volume, blood pressure, and sodium homeostasis.

Indexed as

Nuclear ProteinsAldosteroneAnimalsCell LineCloning, MolecularEpithelial Sodium ChannelsFemaleHumansImmediate-Early ProteinsIon Channel GatingKidneyMolecular Sequence DataOocytesProtein Serine-Threonine KinasesRatsRecombinant ProteinsAldosteroneEpithelial Sodium ChannelsImmediate-Early ProteinsNuclear ProteinsProtein Serine-Threonine KinasesRecombinant ProteinsSerum-Glucocorticoid Regulated KinasesSodiumSodium Channels

Identifiers

PMID10051674
PMCPMC26816
OpenAlexW1977518774

What OpenQuestion holds

Texttitle and abstract
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.