Evidence map›Paper›PMID 24658302›Full record

ArticleDiabetes2014

Role of BH3-only molecules Bim and Puma in β-cell death in Pdx1 deficiency.

Decheng Ren, Juan Sun, Changzheng Wang, Honggang Ye, Liqun Mao, Emily H Cheng, Graeme I Bell, Kenneth S Polonsky

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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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 2 institutions in 1 country.

Decheng RenDepartment of Medicine, University of Chicago, Chicago, IL polonsky@bsd.uchicago.edu decheng@uchicago.edu.
Juan SunDepartment of Medicine, University of Chicago, Chicago, IL.
Changzheng WangDepartment of Medicine, University of Chicago, Chicago, IL.
Honggang YeDepartment of Medicine, University of Chicago, Chicago, IL.
Liqun MaoDepartment of Medicine, University of Chicago, Chicago, IL.
Emily H ChengHuman Oncology and Pathogenesis Program and Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY.
Graeme I BellDepartment of Medicine, University of Chicago, Chicago, IL.
Kenneth S PolonskyDepartment of Medicine, University of Chicago, Chicago, IL polonsky@bsd.uchicago.edu decheng@uchicago.edu.
University of Chicago · USMemorial Sloan Kettering Cancer Center · US

Funding

Pilot and Feasibility ProgramP30DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI Matthew J Brady · 2013 to 2026
$20.9M
Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
THE REGULATION OF HEPATIC INSULIN EXTRACTIONR01DK031842 · NIDDK · WASHINGTON UNIVERSITY · PI POLONSKY, KENNETH S · 1986 to 2013
$4.4M
Apoptotic Network Integrated at the MitochondrionR01CA125562 · NCI · WASHINGTON UNIVERSITY · PI CHENG, EMILY H · 2007 to 2020
$3.4M
NCATS NIH HHS UL1 TR000430NCI NIH HHS R01 CA125562NIDDK NIH HHS P30 DK020595NIDDK NIH HHS P30-DK020595NIDDK NIH HHS R01 DK031842NIDDK NIH HHS R01-DK031842
6 · The paper itself

Abstract

Mutations in pancreatic duodenal homeobox-1 (PDX1) are associated with diabetes in humans. Pdx1-haploinsufficient mice develop diabetes due to an increase in β-cell death leading to reduced β-cell mass. For definition of the molecular link between Pdx1 deficiency and β-cell death, Pdx1-haploinsufficient mice in which the genes for the BH3-only molecules Bim and Puma had been ablated were studied on a high-fat diet. Compared with Pdx1(+/-) mice, animals haploinsufficient for both Pdx1 and Bim or Puma genes showed improved glucose tolerance, enhanced β-cell mass, and reduction in the number of TUNEL-positive cells in islets. These results suggest that Bim and Puma ablation improves β-cell survival in Pdx1(+/-) mice. For exploration of the mechanisms responsible for these findings, Pdx1 gene expression was knocked down in mouse MIN6 insulinoma cells resulting in apoptotic cell death that was found to be associated with increased expression of BH3-only molecules Bim and Puma. If the upregulation of Bim and Puma that occurs during Pdx1 suppression was prevented, apoptotic β-cell death was reduced in vitro. These results suggest that Bim and Puma play an important role in β-cell apoptosis in Pdx1-deficient diabetes.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11Cell LineGene Knockdown TechniquesHaplotypesHomeodomain ProteinsInsulin-Secreting CellsLentivirusMembrane ProteinsMiceProto-Oncogene ProteinsRNA InterferenceRNA, MessengerRNA, Small InterferingApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl2l11 protein, mouseBcl-2-Like Protein 11Homeodomain ProteinsMembrane Proteinspancreatic and duodenal homeobox 1 proteinProto-Oncogene ProteinsPUMA protein, mouseRNA, MessengerRNA, Small InterferingTrans-ActivatorsTumor Suppressor Proteins

Identifiers

PMID24658302
PMCPMC4113059
OpenAlexW2115317450

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.