Evidence map›Paper›PMID 33205075›Full record

ArticleCell reports. Medicine2020

Coxsackievirus B Type 4 Infection in β Cells Downregulates the Chaperone Prefoldin URI to Induce a MODY4-like Diabetes via

Hugo Bernard, Ana Teijeiro, Almudena Chaves-Pérez, Cristian Perna, Basanthi Satish, Anna Novials, Jennifer P Wang, Nabil Djouder

Open access · goldAbstract read
In one paragraph

Article in Cell reports. Medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-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

17 citing papers in PubMed, 17 citations in OpenAlex.

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  17. Epigenetic Regulation of PDX-1 in Type 2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021
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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 4 institutions in 2 countries.

Hugo BernardMolecular Oncology Programme, Growth Factors, Nutrients and Cancer Group, Centro Nacional de Investigaciones Oncológicas, CNIO, Madrid 28029, Spain.
Ana TeijeiroMolecular Oncology Programme, Growth Factors, Nutrients and Cancer Group, Centro Nacional de Investigaciones Oncológicas, CNIO, Madrid 28029, Spain.
Almudena Chaves-PérezMolecular Oncology Programme, Growth Factors, Nutrients and Cancer Group, Centro Nacional de Investigaciones Oncológicas, CNIO, Madrid 28029, Spain.
Cristian PernaDepartment of Pathology, Hospital Universitario Ramón y Cajal, IRYCIS, Madrid 28034, Spain.
Basanthi SatishDepartment of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Anna NovialsIDIBAPS, August Pi i Sunyer Biomedical Research Institute and, CIBERDEM, Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders, Barcelona, Spain.
Jennifer P WangDepartment of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Nabil DjouderMolecular Oncology Programme, Growth Factors, Nutrients and Cancer Group, Centro Nacional de Investigaciones Oncológicas, CNIO, Madrid 28029, Spain.
Spanish National Cancer Research Centre · ESUniversity of Massachusetts Chan Medical School · USInstituto Ramón y Cajal de Investigación Sanitaria · ESSpanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition · ES

Funding

Innate mechanisms for virus-induced diabetesR01AI116920 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WANG, JENNIFER P · 2016 to 2019
$2.0M
NIAID NIH HHS R01 AI116920
6 · The paper itself

Abstract

Enteroviruses are suspected to contribute to insulin-producing β cell loss and hyperglycemia-induced diabetes. However, mechanisms are not fully defined. Here, we show that coxsackievirus B type 4 (CVB4) infection in human islet-engrafted mice and in rat insulinoma cells displays loss of unconventional prefoldin RPB5 interactor (URI) and PDX1, affecting β cell function and identity. Genetic URI ablation in the mouse pancreas causes PDX1 depletion in β cells. Importantly, diabetic PDX1 heterozygous mice overexpressing URI in β cells are more glucose tolerant. Mechanistically, URI loss triggers estrogen receptor nuclear translocation leading to DNA methyltransferase 1 (DNMT1) expression, which induces

Indexed as

AnimalsCapsid ProteinsCoxsackievirus InfectionsDiabetes Mellitus, Type 2Disease Models, AnimalDNA (Cytosine-5-)-Methyltransferase 1Enterovirus B, HumanFemaleGene Expression RegulationGlucoseHomeodomain ProteinsHumansInsulin-Secreting CellsMaleMiceMice, TransgenicCapsid ProteinsDNA (Cytosine-5-)-Methyltransferase 1Dnmt1 protein, mouseGlucoseHomeodomain Proteinspancreatic and duodenal homeobox 1 proteinProcainamideRepressor ProteinsTrans-ActivatorsUri1 protein, mouseVP1 protein, enterovirus Bbeta cellscoxsackievirus B Type 4diabetesDNMT1enterovirusesestrogen receptorhypermethylationPDX1prefoldin URItransdifferentiation

Identifiers

PMID33205075
PMCPMC7659558
OpenAlexW3093712801

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.