Evidence map›Paper›PMID 27229139›Full record

ArticleNucleic acids research2016

Human mutations affect the epigenetic/bookmarking function of HNF1B.

Jonathan Lerner, Alessia Bagattin, Francisco Verdeguer, Munevver P Makinistoglu, Serge Garbay, Tristan Felix, Laurence Heidet, Marco Pontoglio

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 56 citations in OpenAlex.

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  9. Maintaining Transcriptional Specificity Through Mitosis.Annual review of genomics and human genetics · 2022
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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 1 country.

Jonathan LernerDepartment of Development, Reproduction and Cancer, Institut Cochin, INSERM U1016/CNRS UMR 8104/Université Paris-Descartes, Paris 75014, France.
Alessia BagattinDepartment of Development, Reproduction and Cancer, Institut Cochin, INSERM U1016/CNRS UMR 8104/Université Paris-Descartes, Paris 75014, France.
Francisco VerdeguerDepartment of Development, Reproduction and Cancer, Institut Cochin, INSERM U1016/CNRS UMR 8104/Université Paris-Descartes, Paris 75014, France.
Munevver P MakinistogluDepartment of Development, Reproduction and Cancer, Institut Cochin, INSERM U1016/CNRS UMR 8104/Université Paris-Descartes, Paris 75014, France.
Serge GarbayDepartment of Development, Reproduction and Cancer, Institut Cochin, INSERM U1016/CNRS UMR 8104/Université Paris-Descartes, Paris 75014, France.
Tristan FelixDepartment of Development, Reproduction and Cancer, Institut Cochin, INSERM U1016/CNRS UMR 8104/Université Paris-Descartes, Paris 75014, France.
Laurence HeidetDepartment of Pediatric Nephrology, Assistance Publique des Hôpitaux de Paris, Centre de référence des Maladies Rénales Héréditaires de l'Enfant et de l'Adulte (MARHEA), Hospital Necker-Enfants Malades, Paris 75015, France.
Marco PontoglioDepartment of Development, Reproduction and Cancer, Institut Cochin, INSERM U1016/CNRS UMR 8104/Université Paris-Descartes, Paris 75014, France marco.pontoglio@inserm.fr.
Centre National de la Recherche Scientifique · FRUniversité Paris Cité · FRHôpital Necker-Enfants Malades · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bookmarking factors are transcriptional regulators involved in the mitotic transmission of epigenetic information via their ability to remain associated with mitotic chromatin. The mechanisms through which bookmarking factors bind to mitotic chromatin remain poorly understood. HNF1β is a bookmarking transcription factor that is frequently mutated in patients suffering from renal multicystic dysplasia and diabetes. Here, we show that HNF1β bookmarking activity is impaired by naturally occurring mutations found in patients. Interestingly, this defect in HNF1β mitotic chromatin association is rescued by an abrupt decrease in temperature. The rapid relocalization to mitotic chromatin is reversible and driven by a specific switch in DNA-binding ability of HNF1β mutants. Furthermore, we demonstrate that importin-β is involved in the maintenance of the mitotic retention of HNF1β, suggesting a functional link between the nuclear import system and the mitotic localization/translocation of bookmarking factors. Altogether, our studies have disclosed novel aspects on the mechanisms and the genetic programs that account for the mitotic association of HNF1β, a bookmarking factor that plays crucial roles in the epigenetic transmission of information through the cell cycle.

Indexed as

Epigenesis, GeneticAnimalsCells, CulturedChromatinDiabetes Mellitus, Type 2DNADogsEpithelial CellsGene DeletionGreen Fluorescent ProteinsHepatocyte Nuclear Factor 1-betaHeterozygoteHumansKidneyMadin Darby Canine Kidney CellsMitosisChromatinDNAGreen Fluorescent ProteinsHepatocyte Nuclear Factor 1-betaHNF1B protein, humanimportazoleQuinazolinesRecombinant Fusion Proteins

Identifiers

PMID27229139
PMCPMC5041451
OpenAlexW2402201377

What OpenQuestion holds

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LicenceCC BY-NC
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.