Evidence map›Paper›PMID 23617393›Full record

ArticleThe FEBS journal2013

Insulin receptor substrate-2 is expressed in kidney epithelium and up-regulated in diabetic nephropathy.

Michelle B Hookham, Helen C O'Donovan, Rachel H Church, Annie Mercier-Zuber, Lucilla Luzi, Simon P Curran, Rosemarie M Carew, Alejandra Droguett, Sergio Mezzano, Markus Schubert and 3 more

Open access · greenAbstract read
In one paragraph

Article in The FEBS journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. PI3Kinases in Diabetes Mellitus and Its Related Complications.International journal of molecular sciences · 2018
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. 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

13 authors at 7 institutions in 6 countries.

Michelle B HookhamCentre for Vision and Vascular Science, Queen's University Belfast, UK.
Helen C O'Donovan
Rachel H Church
Annie Mercier-Zuber
Lucilla Luzi
Simon P Curran
Rosemarie M Carew
Alejandra Droguett
Sergio Mezzano
Markus Schubert
Morris F White
John K Crean
Derek P Brazil
University College Dublin · IEQueen's University Belfast · GBAustral University of Chile · CLEuropean Institute of Oncology · ITHoward Hughes Medical Institute · USUniversity of Cambridge · GBUniversity of Cologne · DE

Funding

Regulating IRS-proteins by Ser/Thr PhosphorylationR01DK038712 · NIDDK · JOSLIN DIABETES CENTER · PI WHITE, MORRIS F. · 1992 to 2014
$5.0M
Metabolic Crosstalk During Hepatic Insulin ResistanceR01DK098655 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI WHITE, MORRIS F. · 2013 to 2020
$4.0M
Biotechnology and Biological Sciences Research CouncilNIDDK NIH HHS R01 DK038712NIDDK NIH HHS R01 DK098655
6 · The paper itself

Abstract

Diabetic nephropathy (DN) is a progressive fibrotic condition that may lead to end-stage renal disease and kidney failure. Transforming growth factor-β1 and bone morphogenetic protein-7 (BMP7) have been shown to induce DN-like changes in the kidney and protect the kidney from such changes, respectively. Recent data identified insulin action at the level of the nephron as a crucial factor in the development and progression of DN. Insulin requires a family of insulin receptor substrate (IRS) proteins for its physiological effects, and many reports have highlighted the role of insulin and IRS proteins in kidney physiology and disease. Here, we observed IRS2 expression predominantly in the developing and adult kidney epithelium in mouse and human. BMP7 treatment of human kidney proximal tubule epithelial cells (HK-2 cells) increases IRS2 transcription. In addition, BMP7 treatment of HK-2 cells induces an electrophoretic shift in IRS2 migration on SDS/PAGE, and increased association with phosphatidylinositol-3-kinase, probably due to increased tyrosine/serine phosphorylation. In a cohort of DN patients with a range of chronic kidney disease severity, IRS2 mRNA levels were elevated approximately ninefold, with the majority of IRS2 staining evident in the kidney tubules in DN patients. These data show that IRS2 is expressed in the kidney epithelium and may play a role in the downstream protective events triggered by BMP7 in the kidney. The specific up-regulation of IRS2 in the kidney tubules of DN patients also indicates a novel role for IRS2 as a marker and/or mediator of human DN progression.

Indexed as

Gene ExpressionAdolescentAdultAnimalsBase SequenceBinding SitesBone Morphogenetic Protein 7Case-Control StudiesCell LineChildDiabetic NephropathiesEpitheliumFemaleHumansInsulin Receptor Substrate ProteinsKidney TubulesBMP7 protein, humanBone Morphogenetic Protein 7Insulin Receptor Substrate ProteinsIRS2 protein, humanSmad4 ProteinSMAD4 protein, humanbone morphogenetic proteindiabetesinsulin receptor substratekidneynephropathy

Identifiers

PMID23617393
PMCPMC4022317
OpenAlexW1964644144

What OpenQuestion holds

Textmetadata
LicenceTDM
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.