Evidence map›Paper›PMID 33880624›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2021

Alternative exon splicing and differential expression in pancreatic islets reveals candidate genes and pathways implicated in early diabetes development.

Sayeed Ur Rehman, Tanja Schallschmidt, Axel Rasche, Birgit Knebel, Torben Stermann, Delsi Altenhofen, Ralf Herwig, Annette Schürmann, Alexandra Chadt, Hadi Al-Hasani

Open access · hybridAbstract read
In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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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

10 authors at 4 institutions in 2 countries.

Sayeed Ur Rehman *Institute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Duesseldorf, Germany.
Tanja Schallschmidt *Institute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Duesseldorf, Germany.
Axel RascheDepartment of Computational Molecular Biology, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Birgit KnebelInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Duesseldorf, Germany.
Torben StermannInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Duesseldorf, Germany.
Delsi AltenhofenInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Duesseldorf, Germany.
Ralf HerwigDepartment of Computational Molecular Biology, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Annette SchürmannGerman Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Alexandra ChadtInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Duesseldorf, Germany.
Hadi Al-HasaniInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Duesseldorf, Germany. hadi.al-hasani@ddz.de.
German Center for Diabetes Research · DEDeutsches Diabetes-Zentrum e.V. · DEMax Planck Institute for Molecular Genetics · DEGerman Institute of Human Nutrition · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes (T2D) has a strong genetic component. Most of the gene variants driving the pathogenesis of T2D seem to target pancreatic β-cell function. To identify novel gene variants acting at early stage of the disease, we analyzed whole transcriptome data to identify differential expression (DE) and alternative exon splicing (AS) transcripts in pancreatic islets collected from two metabolically diverse mouse strains at 6 weeks of age after three weeks of high-fat-diet intervention. Our analysis revealed 1218 DE and 436 AS genes in islets from NZO/Hl vs C3HeB/FeJ. Whereas some of the revealed genes present well-established markers for β-cell failure, such as Cd36 or Aldh1a3, we identified numerous DE/AS genes that have not been described in context with β-cell function before. The gene Lgals2, previously associated with human T2D development, was DE as well as AS and localizes in a quantitative trait locus (QTL) for blood glucose on Chr.15 that we reported recently in our N

Indexed as

AdipogenesisAlternative SplicingAnimalsBlood GlucoseCD36 AntigensDiabetes Mellitus, Type 2ExonsGalectin 2Gene Expression RegulationHumansInsulinInsulin-Secreting CellsIslets of LangerhansMetabolic Networks and PathwaysMicePPAR gammaBlood GlucoseCD36 AntigensGalectin 2InsulinPPAR gammaPparg protein, mouseretinaldehyde dehydrogenase 3, mouseRetinal Dehydrogenase

Identifiers

PMID33880624
PMCPMC8128753
OpenAlexW3153820878

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.