Evidence map›Paper›PMID 20880397›Full record

ArticleBritish journal of pharmacology2010

Effects of nominally selective inhibitors of the kinases PI3K, SGK1 and PKB on the insulin-dependent control of epithelial Na+ absorption.

Morag K Mansley, Stuart M Wilson

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  6. Article
  7. Review
  8. Review
  9. Trichostatin A blocks aldosterone-induced NaBritish journal of pharmacology · 2019
    Article
  10. Article
  11. Up-regulation of the kinase geneThe Journal of biological chemistry · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. SGK1: The Dark Side of PI3K Signaling.Current topics in developmental biology · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Regulation of ENaC in mice lacking renal insulin receptors in the collecting duct.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    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

2 authors at 1 institution in 1 country.

Morag K MansleyCentre for Cardiovascular and Lung Biology, Division of Medical Sciences, College of Medicine, Dentistry and Nursing, University of Dundee, Dundee, UK.
Stuart M Wilson
University of Dundee · GB

Funding

Medical Research Council G0501531
6 · The paper itself

Abstract

background and purposeInsulin-induced Na(+) retention in the distal nephron may contribute to the development of oedema/hypertension in patients with type 2 diabetes. This response to insulin is usually attributed to phosphatidylinositol-3-kinase (PI3K)/serum and glucocorticoid-inducible kinase 1 (SGK1) but a role for protein kinase B (PKB) has been proposed. The present study therefore aimed to clarify the way in which insulin can evoke Na(+) retention. EXPERIMENTAL APPROACH: We examined the effects of nominally selective inhibitors of PI3K (wortmannin, PI103, GDC-0941), SGK1 (GSK650394A) and PKB (Akti-1/2) on Na(+) transport in hormone-deprived and insulin-stimulated cortical collecting duct (mpkCCD) cells, while PI3K, SGK1 and PKB activities were assayed by monitoring the phosphorylation of endogenous proteins. KEY

resultsWortmannin substantially inhibited basal Na(+) transport whereas PI103 and GDC-0941 had only very small effects. However, these PI3K inhibitors all abolished insulin-induced Na(+) absorption and inactivated PI3K, SGK1 and PKB fully. GSK650394A and Akti-1/2 also inhibited insulin-evoked Na(+) absorption and while GSK650394A inhibited SGK1 without affecting PKB, Akti-1/2 inactivated both kinases. CONCLUSION AND IMPLICATIONS: While studies undertaken using PI103 and GDC-0941 show that hormone-deprived cells can absorb Na(+) independently of PI3K, PI3K seems to be essential for insulin induced Na(+) transport. Akti-1/2 does not act as a selective inhibitor of PKB and data obtained using this compound must therefore be treated with caution. GSK650394A, on the other hand, selectively inhibits SGK1 and the finding that GSK650394A suppressed insulin-induced Na(+) absorption suggests that this response is dependent upon signalling via PI3K/SGK1.

Indexed as

Phosphoinositide-3 Kinase InhibitorsAbsorptionAndrostadienesAnimalsBenzoatesBenzylaminesBridged Bicyclo Compounds, HeterocyclicCells, CulturedEpithelial CellsFuransImmediate-Early ProteinsIndazolesInsulinIon TransportKidney Tubules, CollectingMembrane Potentials2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidine2-cyclopentyl-4-(5-phenyl-1H-pyrrolo(2,3-b)pyridin-3-yl)-benzoic acidAkt-I-1,2 compoundAndrostadienesBenzoatesBenzylaminesBridged Bicyclo Compounds, HeterocyclicFuransImmediate-Early ProteinsIndazolesInsulinPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPI103Protein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPyridinesPyrimidinesQuinoxalinesSerum-Glucocorticoid Regulated KinasesSodiumSulfonamidesWortmannin

Identifiers

PMID20880397
PMCPMC2990156
OpenAlexW1604894935

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.