Evidence map›Paper›PMID 25171524›Full record

ArticleBioEssays : news and reviews in molecular, cellular and developmental biology2014

Mitosis, double strand break repair, and telomeres: a view from the end: how telomeres and the DNA damage response cooperate during mitosis to maintain genome stability.

Anthony J Cesare

Open access · hybridAbstract read
In one paragraph

Article in BioEssays : news and reviews in molecular, cellular and developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

Anthony J CesareChildren's Medical Research Institute, Genome Integrity Group, Westmead, NSW, Australia; University of Sydney, Sydney Medical School, Sydney, NSW, Australia.
Children's Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Double strand break (DSB) repair is suppressed during mitosis because RNF8 and downstream DNA damage response (DDR) factors, including 53BP1, do not localize to mitotic chromatin. Discovery of the mitotic kinase-dependent mechanism that inhibits DSB repair during cell division was recently reported. It was shown that restoring mitotic DSB repair was detrimental, resulting in repair dependent genome instability and covalent telomere fusions. The telomere DDR that occurs naturally during cellular aging and in cancer is known to be refractory to G2/M checkpoint activation. Such DDR-positive telomeres, and those that occur as part of the telomere-dependent prolonged mitotic arrest checkpoint, normally pass through mitosis without covalent ligation, but result in cell growth arrest in G1 phase. The discovery that suppressing DSB repair during mitosis may function primarily to protect DDR-positive telomeres from fusing during cell division reinforces the unique cooperation between telomeres and the DDR to mediate tumor suppression.

Indexed as

DNA Breaks, Double-StrandedChromatinDNA-Binding ProteinsDNA RepairG1 Phase Cell Cycle CheckpointsGenomic InstabilityHumansIntracellular Signaling Peptides and ProteinsMitosisPhosphorylationTelomereTumor Suppressor p53-Binding Protein 1UbiquitinationUbiquitin-Protein LigasesChromatinDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsRNF8 protein, humanTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1Ubiquitin-Protein Ligasescell cycleDNA damage responsedouble strand break repairmitosistelomeres

Identifiers

PMID25171524
PMCPMC4270212
OpenAlexW2140679171

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.