Evidence map›Paper›PMID 27806100›Full record

ArticlePloS one2016

Transcriptional Activation of Pericentromeric Satellite Repeats and Disruption of Centromeric Clustering upon Proteasome Inhibition.

Theona Natisvili, Cihangir Yandim, Raquel Silva, Giulia Emanuelli, Felix Krueger, Sathiji Nageshwaran, Richard Festenstein

Abstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
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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

7 authors.

Theona NatisviliGene Control Mechanisms and Disease Group, Department of Medicine, Division of Brain Sciences and MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Cihangir YandimGene Control Mechanisms and Disease Group, Department of Medicine, Division of Brain Sciences and MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Raquel SilvaGene Control Mechanisms and Disease Group, Department of Medicine, Division of Brain Sciences and MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Giulia EmanuelliGene Control Mechanisms and Disease Group, Department of Medicine, Division of Brain Sciences and MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Felix KruegerBioinformatics Group, Babraham Institute, Cambridge, United Kingdom.
Sathiji NageshwaranGene Control Mechanisms and Disease Group, Department of Medicine, Division of Brain Sciences and MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Richard FestensteinGene Control Mechanisms and Disease Group, Department of Medicine, Division of Brain Sciences and MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, United Kingdom.

Funding

Medical Research Council MC_U120081321Medical Research Council MR/J007943/1Wellcome Trust
6 · The paper itself

Abstract

Heterochromatinisation of pericentromeres, which in mice consist of arrays of major satellite repeats, are important for centromere formation and maintenance of genome stability. The dysregulation of this process has been linked to genomic stress and various cancers. Here we show in mice that the proteasome binds to major satellite repeats and proteasome inhibition by MG132 results in their transcriptional de-repression; this de-repression is independent of cell-cycle perturbation. The transcriptional activation of major satellite repeats upon proteasome inhibition is accompanied by delocalisation of heterochromatin protein 1 alpha (HP1α) from chromocentres, without detectable change in the levels of histone H3K9me3, H3K4me3, H3K36me3 and H3 acetylation on the major satellite repeats. Moreover, inhibition of the proteasome was found to increase the number of chromocentres per cell, reflecting destabilisation of the chromocentre structures. Our findings suggest that the proteasome plays a role in maintaining heterochromatin integrity of pericentromeres.

Indexed as

AcetylationAnimalsCentromereChromatinChromobox Protein Homolog 5Chromosomal InstabilityChromosomal Proteins, Non-HistoneDNA, SatelliteHistonesIn Situ Hybridization, FluorescenceLeupeptinsMiceNIH 3T3 CellsProteasome Endopeptidase ComplexTranscription, Geneticbenzyloxycarbonylleucyl-leucyl-leucine aldehydeChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDNA, SatelliteHistonesLeupeptinsProteasome Endopeptidase Complex

Identifiers

PMID27806100
PMCPMC5091837

What OpenQuestion holds

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LicenceCC BY
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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.