Evidence map›Paper›PMID 26400768›Full record

ArticleScientific reports2015

DNAJB3/HSP-40 cochaperone improves insulin signaling and enhances glucose uptake in vitro through JNK repression.

Mohamed Abu-Farha, Preethi Cherian, Irina Al-Khairi, Ali Tiss, Abdelkrim Khadir, Sina Kavalakatt, Samia Warsame, Mohammed Dehbi, Kazem Behbehani, Jehad Abubaker

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

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    Article
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  20. Evidence-based complementary and alternative medicine : eCAM · 2017
    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

10 authors at 2 institutions in 2 countries.

Mohamed Abu-FarhaBiochemistry and Molecular Biology unit, Dasman Diabetes Institute, Kuwait.
Preethi CherianBiochemistry and Molecular Biology unit, Dasman Diabetes Institute, Kuwait.
Irina Al-KhairiBiochemistry and Molecular Biology unit, Dasman Diabetes Institute, Kuwait.
Ali TissBiochemistry and Molecular Biology unit, Dasman Diabetes Institute, Kuwait.
Abdelkrim KhadirBiochemistry and Molecular Biology unit, Dasman Diabetes Institute, Kuwait.
Sina KavalakattBiochemistry and Molecular Biology unit, Dasman Diabetes Institute, Kuwait.
Samia WarsameBiochemistry and Molecular Biology unit, Dasman Diabetes Institute, Kuwait.
Mohammed DehbiDiabetes Research Center, Qatar Biomedical Research Institute, Education City, Doha, Qatar.
Kazem BehbehaniBiochemistry and Molecular Biology unit, Dasman Diabetes Institute, Kuwait.
Jehad AbubakerBiochemistry and Molecular Biology unit, Dasman Diabetes Institute, Kuwait.
Dasman Diabetes Institute · KWQatar Foundation · QA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heat shock response (HSR) is an essential host-defense mechanism that is dysregulated in obesity-induced insulin resistance and type 2 diabetes (T2D). Our recent data demonstrated that DNAJB3 was downregulated in obese human subjects and showed negative correlation with inflammatory markers. Nevertheless, DNAJB3 expression pattern in diabetic subjects and its mode of action are not yet known. In this study, we showed reduction in DNAJB3 transcript and protein levels in PBMC and subcutaneous adipose tissue of obese T2D compared to obese non-diabetic subjects. Overexpression of DNAJB3 in HEK293 and 3T3-L1 cells reduced JNK, IRS-1 Ser-307 phosphorylation and enhanced Tyr-612 phosphorylation suggesting an improvement in IRS-1 signaling. Furthermore, DNAJB3 mediated the PI3K/AKT pathway activation through increasing AKT and AS160 phosphorylation. AS160 mediates the mobilization of GLUT4 transporter to the cell membrane and thereby improves glucose uptake. Using pre-adipocytes cells we showed that DNAJB3 overexpression caused a significant increase in the glucose uptake, possibly through its phosphorylation of AS160. In summary, our results shed the light on the possible role of DNAJB3 in improving insulin sensitivity and glucose uptake through JNK repression and suggest that DNAJB3 could be a potential target for therapeutic treatment of obesity-induced insulin resistance.

Indexed as

Signal Transduction3T3-L1 CellsAdipose TissueAnimalsCell LineDiabetes Mellitus, Type 2Gene Expression RegulationGlucoseHEK293 CellsHSP40 Heat-Shock ProteinsHumansInsulinJNK Mitogen-Activated Protein KinasesLeukocytes, MononuclearMiceModels, BiologicalDNAJB3 protein, humanGlucoseHSP40 Heat-Shock ProteinsInsulinJNK Mitogen-Activated Protein Kinases

Identifiers

PMID26400768
PMCPMC4585859
OpenAlexW2283126157

What OpenQuestion holds

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Registered trials

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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.