Evidence map›Paper›PMID 26544937›Full record

ArticleCell2015

53BP1 and the LINC Complex Promote Microtubule-Dependent DSB Mobility and DNA Repair.

Francisca Lottersberger, Roos Anna Karssemeijer, Nadya Dimitrova, Titia de Lange

Abstract read
In one paragraph

Article in Cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers.

0numbers the graph read from it
0cells of the map it votes in
206citing 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

206 citing papers in PubMed.

  1. Kinetic Control of Condensate Function: How the Formation Dynamics of APBs Influence ALT Cancer Telomere Length Heterogeneity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  2. Review
  3. Article
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  5. Integrative modeling of the genome structure and dynamics in fission yeast.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. The Polymers of Life: Exploring Cellular Function Through Polymer Concepts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  8. Article
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146 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

4 authors.

Francisca LottersbergerLaboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Roos Anna KarssemeijerLaboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Nadya DimitrovaLaboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Titia de LangeLaboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA. Electronic address: delange@rockefeller.edu.

Funding

Regulation of DSB repair by 53BP1R01CA181090 · NCI · ROCKEFELLER UNIVERSITY · PI DE LANGE, TITIA · 2014 to 2016
$1.4M
NCI NIH HHS 5R01CA181090NCI NIH HHS R01 CA181090
6 · The paper itself

Abstract

Increased mobility of chromatin surrounding double-strand breaks (DSBs) has been noted in yeast and mammalian cells but the underlying mechanism and its contribution to DSB repair remain unclear. Here, we use a telomere-based system to track DNA damage foci with high resolution in living cells. We find that the greater mobility of damaged chromatin requires 53BP1, SUN1/2 in the linker of the nucleoskeleton, and cytoskeleton (LINC) complex and dynamic microtubules. The data further demonstrate that the excursions promote non-homologous end joining of dysfunctional telomeres and implicated Nesprin-4 and kinesins in telomere fusion. 53BP1/LINC/microtubule-dependent mobility is also evident at irradiation-induced DSBs and contributes to the mis-rejoining of drug-induced DSBs in BRCA1-deficient cells showing that DSB mobility can be detrimental in cells with numerous DSBs. In contrast, under physiological conditions where cells have only one or a few lesions, DSB mobility is proposed to prevent errors in DNA repair.

Indexed as

DNA Breaks, Double-StrandedDNA RepairAnimalsCarrier ProteinsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsDNA End-Joining RepairHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsMiceMice, KnockoutMicrotubule-Associated ProteinsMicrotubulesNuclear ProteinsPhosphorylationCarrier ProteinsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicrotubule-Associated ProteinsNuclear ProteinsPaxip1 protein, mouseSUN1 protein, mouseSun2 protein, mouseTelomere-Binding ProteinsTelomeric Repeat Binding Protein 2TERF2 protein, humanTP53BP1 protein, humanTrp53bp1 protein, mouseTumor Suppressor p53-Binding Protein 1

Identifiers

PMID26544937
PMCPMC4636737

What OpenQuestion holds

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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.