Evidence map›Paper›PMID 37689751›Full record

ArticleNature communications2023

NEUROD1 reinforces endocrine cell fate acquisition in pancreatic development.

Romana Bohuslavova, Valeria Fabriciova, Ondrej Smolik, Laura Lebrón-Mora, Pavel Abaffy, Sarka Benesova, Daniel Zucha, Lukas Valihrach, Zuzana Berkova, Frantisek Saudek and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
12.4field-weighted citation impact, top 1% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

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  9. Congenital hyperinsulinism due to NEUROD1 gene mutation.Annals of pediatric endocrinology & metabolism · 2025
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  12. Review
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  15. Case Report:Frontiers in endocrinology · 2025
    Article
  16. Integrating Prior Knowledge Using Transformer for Gene Regulatory Network Inference.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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  18. 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

11 authors at 2 institutions in 1 country.

Romana Bohuslavova *Laboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, 25250, Vestec, Czechia.ORCID http://orcid.org/0000-0001-6110-4688
Valeria Fabriciova *Laboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, 25250, Vestec, Czechia.
Ondrej Smolik *Laboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, 25250, Vestec, Czechia.ORCID http://orcid.org/0000-0003-1250-2684
Laura Lebrón-MoraLaboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, 25250, Vestec, Czechia.ORCID http://orcid.org/0009-0002-6250-1217
Pavel AbaffyLaboratory of Gene Expression, Institute of Biotechnology CAS, 25250, Vestec, Czechia.ORCID http://orcid.org/0000-0002-7571-8880
Sarka BenesovaLaboratory of Gene Expression, Institute of Biotechnology CAS, 25250, Vestec, Czechia.ORCID http://orcid.org/0000-0003-3956-5968
Daniel ZuchaLaboratory of Gene Expression, Institute of Biotechnology CAS, 25250, Vestec, Czechia.ORCID http://orcid.org/0000-0002-2469-1315
Lukas ValihrachLaboratory of Gene Expression, Institute of Biotechnology CAS, 25250, Vestec, Czechia.ORCID http://orcid.org/0000-0002-6704-4337
Zuzana BerkovaDiabetes Centre, Experimental Medicine Centre, Institute for Clinical and Experimental Medicine, 14021, Prague, Czechia.ORCID http://orcid.org/0000-0001-8053-9978
Frantisek SaudekDiabetes Centre, Experimental Medicine Centre, Institute for Clinical and Experimental Medicine, 14021, Prague, Czechia.
Gabriela PavlinkovaLaboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, 25250, Vestec, Czechia. gpavlinkova@ibt.cas.cz.ORCID http://orcid.org/0000-0002-5689-6577
Czech Academy of Sciences, Institute of Biotechnology · CZInstitute of Clinical and Experimental Medicine · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NEUROD1 is a transcription factor that helps maintain a mature phenotype of pancreatic β cells. Disruption of Neurod1 during pancreatic development causes severe neonatal diabetes; however, the exact role of NEUROD1 in the differentiation programs of endocrine cells is unknown. Here, we report a crucial role of the NEUROD1 regulatory network in endocrine lineage commitment and differentiation. Mechanistically, transcriptome and chromatin landscape analyses demonstrate that Neurod1 inactivation triggers a downregulation of endocrine differentiation transcription factors and upregulation of non-endocrine genes within the Neurod1-deficient endocrine cell population, disturbing endocrine identity acquisition. Neurod1 deficiency altered the H3K27me3 histone modification pattern in promoter regions of differentially expressed genes, which resulted in gene regulatory network changes in the differentiation pathway of endocrine cells, compromising endocrine cell potential, differentiation, and functional properties.

Indexed as

Endocrine CellsInsulin-Secreting CellsCell DifferentiationTranscriptional ActivationTranscription FactorsTranscription Factors

Identifiers

PMID37689751
PMCPMC10492842
OpenAlexW4386579580

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.