Evidence map›Paper›PMID 28985358›Full record

ArticleNucleic acids research2017

Identification of Plagl1/Zac1 binding sites and target genes establishes its role in the regulation of extracellular matrix genes and the imprinted gene network.

Annie Varrault, Christelle Dantec, Anne Le Digarcher, Laëtitia Chotard, Benoit Bilanges, Hugues Parrinello, Emeric Dubois, Stéphanie Rialle, Dany Severac, Tristan Bouschet and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 69 citations in OpenAlex.

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  13. The imprinted gene Zac1 regulates steatosis in developmental cadmium-induced nonalcoholic fatty liver disease.Toxicological sciences : an official journal of the Society of Toxicology · 2023
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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 1 institution in 1 country.

Annie VarraultInstitut de Génomique Fonctionnelle, IGF, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
Christelle DantecMontpellier GenomiX, MGX, BioCampus Montpellier, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
Anne Le DigarcherInstitut de Génomique Fonctionnelle, IGF, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
Laëtitia ChotardInstitut de Génomique Fonctionnelle, IGF, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
Benoit BilangesInstitut de Génomique Fonctionnelle, IGF, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
Hugues ParrinelloMontpellier GenomiX, MGX, BioCampus Montpellier, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
Emeric DuboisMontpellier GenomiX, MGX, BioCampus Montpellier, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
Stéphanie RialleMontpellier GenomiX, MGX, BioCampus Montpellier, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
Dany SeveracMontpellier GenomiX, MGX, BioCampus Montpellier, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
Tristan BouschetInstitut de Génomique Fonctionnelle, IGF, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
Laurent JournotInstitut de Génomique Fonctionnelle, IGF, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PLAGL1/ZAC1 undergoes parental genomic imprinting, is paternally expressed, and is a member of the imprinted gene network (IGN). It encodes a zinc finger transcription factor with anti-proliferative activity and is a candidate tumor suppressor gene on 6q24 whose expression is frequently lost in various neoplasms. Conversely, gain of PLAGL1 function is responsible for transient neonatal diabetes mellitus, a rare genetic disease that results from defective pancreas development. In the present work, we showed that Plagl1 up-regulation was not associated with DNA damage-induced cell cycle arrest. It was rather associated with physiological cell cycle exit that occurred with contact inhibition, growth factor withdrawal, or cell differentiation. To gain insights into Plagl1 mechanism of action, we identified Plagl1 target genes by combining chromatin immunoprecipitation and genome-wide transcriptomics in transfected cell lines. Plagl1-elicited gene regulation correlated with multiple binding to the proximal promoter region through a GC-rich motif. Plagl1 target genes included numerous genes involved in signaling, cell adhesion, and extracellular matrix composition, including collagens. Plagl1 targets also included 22% of the 409 genes that make up the IGN. Altogether, this work identified Plagl1 as a transcription factor that coordinated the regulation of a subset of IGN genes and controlled extracellular matrix composition.

Indexed as

Gene Expression Regulation, DevelopmentalGenomic ImprintingAnimalsAnimals, NewbornBinding SitesCell Cycle ProteinsCells, CulturedEmbryo, MammalianExtracellular MatrixGene Regulatory NetworksHumansMaleMiceMice, Inbred C57BLProtein BindingTranscription FactorsCell Cycle ProteinsPLAGL1 protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID28985358
PMCPMC5737700
OpenAlexW2740664637

What OpenQuestion holds

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LicenceCC BY-NC
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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.