Evidence map›Paper›PMID 21605081›Full record

ArticleThe Biochemical journal2011

Liver-specific deletion of protein tyrosine phosphatase (PTP) 1B improves obesity- and pharmacologically induced endoplasmic reticulum stress.

Abdelali Agouni, Nimesh Mody, Carl Owen, Alicja Czopek, Derek Zimmer, Mohamed Bentires-Alj, Kendra K Bence, Mirela Delibegović

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 110 citations in OpenAlex.

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  10. Inhibition of the PI 3-kinase pathway disrupts the unfolded protein response and reduces sensitivity to ER stress-dependent apoptosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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  13. Ablation ofDisease models & mechanisms · 2020
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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

8 authors at 1 institution in 1 country.

Abdelali AgouniInstitute of Biological and Environmental Sciences, College of Life Sciences and Medicine, University of Aberdeen, UK.
Nimesh Mody
Carl Owen
Alicja Czopek
Derek Zimmer
Mohamed Bentires-Alj
Kendra K Bence
Mirela Delibegović
Friedrich Miescher Institute · CH

Funding

Neuronal Protein Tyrosine Phosphatases in MetabolismR01DK082417 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI BENCE, KENDRA · 2009 to 2015
$2.6M
Biotechnology and Biological Sciences Research CouncilBritish Heart FoundationNIDDK NIH HHS R01 DK082417NIDDK NIH HHS R01DK082417
6 · The paper itself

Abstract

Obesity is associated with induction of the ER (endoplasmic reticulum)-stress response signalling and insulin resistance. PTP1B (protein tyrosine phosphatase 1B) is a major regulator of adiposity and insulin sensitivity. The aim of the present study was to investigate the role of L-PTP1B (liver-specific PTP1B) in chronically HFD (high-fat diet) and pharmacologically induced (tunicamycin and thapsigargin) ER-stress response signalling in vitro and in vivo. We assessed the effects of ER-stress response induction on hepatic PTP1B expression, and consequences of hepatic-PTP1B deficiency, in cells and mouse liver, on components of ER-stress response signalling. We found that PTP1B protein and mRNA expression levels were up-regulated in response to acute and/or chronic ER stress, in vitro and in vivo. Silencing PTP1B in hepatic cell lines or mouse liver (L-PTP1B(-/-)) protected against induction of pharmacologically induced and/or obesity-induced ER stress. The HFD-induced increase in CHOP (CCAAT/enhancer-binding protein homologous protein) and BIP (binding immunoglobulin protein) mRNA levels were partially inhibited, whereas ATF4 (activated transcription factor 4), GADD34 (growth-arrest and DNA-damage-inducible protein 34), GRP94 (glucose-regulated protein 94), ERDJ4 (ER-localized DnaJ homologue) mRNAs and ATF6 protein cleavage were completely suppressed in L-PTP1B(-/-) mice relative to control littermates. L-PTP1B(-/-) mice also had increased nuclear translocation of spliced XBP-1 (X box-binding protein-1) via increased p85α binding. We demonstrate that the ER-stress response and L-PTP1B expression are interlinked in obesity- and pharmacologically induced ER stress and this may be one of the mechanisms behind improved insulin sensitivity and lower lipid accumulation in L-PTP1B(-/-) mice.

Indexed as

Gene DeletionStress, PhysiologicalActivating Transcription Factor 6AnimalsCell NucleusClass Ia Phosphatidylinositol 3-KinaseDNA-Binding ProteinsEndoplasmic ReticulumEndoribonucleasesEukaryotic Initiation Factor-2Gene Knockdown TechniquesGlucoseHep G2 CellsHomeostasisHumansLipid MetabolismActivating Transcription Factor 6Class Ia Phosphatidylinositol 3-KinaseDNA-Binding ProteinsEndoribonucleasesErn1 protein, mouseEukaryotic Initiation Factor-2GlucoseProtein Serine-Threonine KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 1Regulatory Factor X Transcription FactorsRNA, MessengerThapsigarginTranscription FactorsTunicamycinX-Box Binding Protein 1XBP1 protein, humanXbp1 protein, mouse

Identifiers

PMID21605081
PMCPMC3744093
OpenAlexW2099513488

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.