Evidence map›Paper›PMID 24204775›Full record

ArticlePloS one2013

Protein tyrosine phosphatase 1B and insulin resistance: role of endoplasmic reticulum stress/reactive oxygen species/nuclear factor kappa B axis.

Evgeniy Panzhinskiy, Jun Ren, Sreejayan Nair

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 99 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Article
  8. Review
  9. Article
  10. Review
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  12. Mechanistic Research into the Effects of the Jianpi Xiaozhi Formula on Liver Injury in Diabetic Rats.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Autoregulation of insulin receptor signaling through MFGE8 and the αvβ5 integrin.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Evaluation of the Hypoglycemic Activity ofFrontiers in pharmacology · 2021
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Evgeniy PanzhinskiySchool of Pharmacy & Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, Wyoming, United States of America.
Jun Ren
Sreejayan Nair
University of Wyoming · US

Funding

Wyoming IDeA Networks of Biomedical Research ExcellenceP20RR016474 · NCRR · UNIVERSITY OF WYOMING · PI REN, JUN · 2001 to 2011
$28.2M
NCRR NIH HHS NIH P20RR016474NCRR NIH HHS P20 RR016474
6 · The paper itself

Abstract

Obesity-induced endoplasmic reticulum (ER) stress has been proposed as an important pathway in the development of insulin resistance. Protein-tyrosine phosphatase 1B (PTP1B) is a negative regulator of insulin signaling and is tethered to the ER-membrane. The aim of the study was to determine the mechanisms involved in the crosstalk between ER-stress and PTP1B. PTP1B whole body knockout and C57BL/6J mice were subjected to a high-fat or normal chow-diet for 20 weeks. High-fat diet feeding induced body weight gain, increased adiposity, systemic glucose intolerance, and hepatic steatosis were attenuated by PTP1B deletion. High-fat diet- fed PTP1B knockout mice also exhibited improved glucose uptake measured using [(3)H]-2-deoxy-glucose incorporation assay and Akt phosphorylation in the skeletal muscle tissue, compared to their wild-type control mice which received similar diet. High-fat diet-induced upregulation of glucose-regulated protein-78, phosphorylation of eukaryotic initiation factor 2α and c-Jun NH2-terminal kinase-2 were significantly attenuated in the PTP1B knockout mice. Mice lacking PTP1B showed decreased expression of the autophagy related protein p62 and the unfolded protein response adaptor protein NCK1 (non-catalytic region of tyrosine kinase). Treatment of C2C12 myotubes with the ER-stressor tunicamycin resulted in the accumulation of reactive oxygen species (ROS), leading to the activation of protein expression of PTP1B. Furthermore, tunicamycin-induced ROS production activated nuclear translocation of NFκB p65 and was required for ER stress-mediated expression of PTP1B. Our data suggest that PTP1B is induced by ER stress via the activation of the ROS-NFκB axis which is causes unfolded protein response and mediates insulin resistance in the skeletal muscle under obese condition.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsDietary FatsDiet, High-FatEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEukaryotic Initiation Factor-2FemaleGene Expression RegulationGlucose IntoleranceHeat-Shock ProteinsInsulin ResistanceJNK Mitogen-Activated Protein KinasesMiceMice, Inbred C57BLAdaptor Proteins, Signal TransducingDietary FatsEndoplasmic Reticulum Chaperone BiPEukaryotic Initiation Factor-2Gtf2h1 protein, mouseHeat-Shock ProteinsJNK Mitogen-Activated Protein KinasesNck proteinNF-kappa BOncogene ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 1Proto-Oncogene Proteins c-aktPtpn1 protein, mouseReactive Oxygen SpeciesTranscription FactorsTranscription Factor TFIIHTunicamycin

Identifiers

PMID24204775
PMCPMC3799617
OpenAlexW2155736856

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.