Evidence map›Paper›PMID 25762097›Full record

ArticleNature communications2015

TOPBP1 recruits TOP2A to ultra-fine anaphase bridges to aid in their resolution.

Ronan Broderick, Jadwiga Nieminuszczy, Andrew N Blackford, Alicja Winczura, Wojciech Niedzwiedz

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 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.1field-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

53 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability.Journal of experimental & clinical cancer research : CR · 2024
    Article
  13. Review
  14. DNA strand breaks at centromeres: Friend or foe?Seminars in cell & developmental biology · 2024
    Review
  15. Article
  16. Pre-rRNA Facilitates TopBP1-Mediated DNA Double-Strand Break Response.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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

5 authors at 1 institution in 1 country.

Ronan BroderickDepartment of Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK.
Jadwiga Nieminuszczy1] Department of Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK [2] Institute of Biochemistry and Biophysics, PAS, 02-106 Warsaw, Poland.
Andrew N BlackfordDepartment of Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK.ORCID 000000031979021X
Alicja WinczuraDepartment of Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK.
Wojciech NiedzwiedzDepartment of Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK.
University of Oxford · GB

Funding

Cancer Research UK 11224Medical Research Council G0902418Medical Research Council MR/K01577X/1Worldwide Cancer Research 07-0922
6 · The paper itself

Abstract

During mitosis, sister chromatids must be faithfully segregated to ensure that daughter cells receive one copy of each chromosome. However, following replication they often remain entangled. Topoisomerase IIα (TOP2A) has been proposed to resolve such entanglements, but the mechanisms governing TOP2A recruitment to these structures remain poorly understood. Here, we identify TOPBP1 as a novel interactor of TOP2A, and reveal that it is required for TOP2A recruitment to ultra-fine anaphase bridges (UFBs) in mitosis. The C-terminal region of TOPBP1 interacts with TOP2A, and TOPBP1 recruitment to UFBs requires its BRCT domain 5. Depletion of TOPBP1 leads to accumulation of UFBs, the majority of which arise from centromeric loci. Accordingly, expression of a TOPBP1 mutant that is defective in TOP2A binding phenocopies TOP2A depletion. These findings provide new mechanistic insights into how TOP2A promotes resolution of UFBs during mitosis, and highlights a pivotal role for TOPBP1 in this process.

Indexed as

AnaphaseGene Expression RegulationAntigens, NeoplasmCarrier ProteinsCell Cycle ProteinsCell Line, TumorCentromereChromatidsChromosomesDNADNA-Binding ProteinsDNA Topoisomerases, Type IIGene Expression Regulation, NeoplasticGreen Fluorescent ProteinsHEK293 CellsHeLa CellsAntigens, NeoplasmCarrier ProteinsCell Cycle ProteinsDNADNA-Binding ProteinsDNA Topoisomerases, Type IIGreen Fluorescent ProteinsNuclear ProteinsPoly-ADP-Ribose Binding ProteinsTOP2A protein, humanTOPBP1 protein, human

Identifiers

PMID25762097
PMCPMC4374157
OpenAlexW1996602584

What OpenQuestion holds

Textmetadata
LicenceTDM
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.