Evidence map›Paper›PMID 26643143›Full record

ArticleNature communications2015

PICH promotes sister chromatid disjunction and co-operates with topoisomerase II in mitosis.

Christian F Nielsen, Diana Huttner, Anna H Bizard, Seiki Hirano, Tian-Neng Li, Timea Palmai-Pallag, Victoria A Bjerregaard, Ying Liu, Erich A Nigg, Lily Hui-Ching Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

79 citing papers in PubMed, 130 citations in OpenAlex.

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  4. Mechanistic basis for relaxation of DNA supercoils by human topoisomerase IIIα-RMI1-RMI2.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  12. DNA strand breaks at centromeres: Friend or foe?Seminars in cell & developmental biology · 2024
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19 more citing papers are in PubMed but not listed here.

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 4 institutions in 6 countries.

Christian F NielsenCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Diana HuttnerCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Anna H BizardCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, DK-2200 Copenhagen, Denmark.ORCID http://orcid.org/0000-0003-1858-3999
Seiki HiranoWeatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, OX3 9DS Oxford, UK.
Tian-Neng LiInstitute of Molecular and Cellular Biology &Department of Medical Science, National Tsing Hua University, 30013 Hsinchu, Taiwan.
Timea Palmai-PallagWeatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, OX3 9DS Oxford, UK.ORCID http://orcid.org/0000-0002-7402-2144
Victoria A BjerregaardCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Ying LiuCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Erich A NiggBiozentrum, University of Basel, CH-4056 Basel, Switzerland.
Lily Hui-Ching WangInstitute of Molecular and Cellular Biology &Department of Medical Science, National Tsing Hua University, 30013 Hsinchu, Taiwan.
Ian D HicksonCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, DK-2200 Copenhagen, Denmark.
University of Copenhagen · DKJohn Radcliffe Hospital · GBUniversity of Basel · CHNational Tsing Hua University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PICH is a SNF2 family DNA translocase that binds to ultra-fine DNA bridges (UFBs) in mitosis. Numerous roles for PICH have been proposed from protein depletion experiments, but a consensus has failed to emerge. Here, we report that deletion of PICH in avian cells causes chromosome structural abnormalities, and hypersensitivity to an inhibitor of Topoisomerase II (Topo II), ICRF-193. ICRF-193-treated PICH(-/-) cells undergo sister chromatid non-disjunction in anaphase, and frequently abort cytokinesis. PICH co-localizes with Topo IIα on UFBs and at the ribosomal DNA locus, and the timely resolution of both structures depends on the ATPase activity of PICH. Purified PICH protein strongly stimulates the catalytic activity of Topo II in vitro. Consistent with this, a human PICH(-/-) cell line exhibits chromosome instability and chromosome condensation and decatenation defects similar to those of ICRF-193-treated cells. We propose that PICH and Topo II cooperate to prevent chromosome missegregation events in mitosis.

Indexed as

AnimalsAntigens, NeoplasmAvian ProteinsBlotting, WesternCell Cycle ProteinsCell Line, TumorChickensChromatidsChromosomal InstabilityChromosome SegregationDNA-Binding ProteinsDNA HelicasesDNA Topoisomerases, Type IIFlow CytometryFluorescent Antibody Technique, IndirectGene Knockout TechniquesAntigens, NeoplasmAvian ProteinsCell Cycle ProteinsDNA-Binding ProteinsDNA HelicasesDNA Topoisomerases, Type IIERCC6L protein, human

Identifiers

PMID26643143
PMCPMC4686863
OpenAlexW2178382809

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Registered trials

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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.