Evidence map›Paper›PMID 26439176›Full record

ArticleDNA repair2015

Efficient cleavage of single and clustered AP site lesions within mono-nucleosome templates by CHO-K1 nuclear extract contrasts with retardation of incision by purified APE1.

Laura J Eccles, Hervé Menoni, Dimitar Angelov, Martine E Lomax, Peter O'Neill

Open access · hybridAbstract read
In one paragraph

Article in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. The Cellular Response to Complex DNA Damage Induced by Ionising Radiation.International journal of molecular sciences · 2023
    Review
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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

5 authors at 2 institutions in 2 countries.

Laura J EcclesCRUK-MRC Oxford Institute for Radiation Oncology, University of Oxford, Old Road Campus Research Building, Roosevelt Drive, Oxford OX3 7DQ, UK.
Hervé MenoniUniversité de Lyon, Laboratoire de Biologie Moléculaire de la Cellule, CNRS-UMR 5239, Ecole Normale Supérieure de Lyon, 69007, France.
Dimitar AngelovUniversité de Lyon, Laboratoire de Biologie Moléculaire de la Cellule, CNRS-UMR 5239, Ecole Normale Supérieure de Lyon, 69007, France.
Martine E LomaxCRUK-MRC Oxford Institute for Radiation Oncology, University of Oxford, Old Road Campus Research Building, Roosevelt Drive, Oxford OX3 7DQ, UK.
Peter O'NeillCRUK-MRC Oxford Institute for Radiation Oncology, University of Oxford, Old Road Campus Research Building, Roosevelt Drive, Oxford OX3 7DQ, UK. Electronic address: peter.oneill@oncology.ox.ac.uk.
University of Oxford · GBUniversité Claude Bernard Lyon 1 · FR

Funding

Medical Research Council MC_PC_12001
6 · The paper itself

Abstract

Clustered DNA damage is a unique characteristic of radiation-induced DNA damage and the formation of these sites poses a serious challenge to the cell's repair machinery. Within a cell DNA is compacted, with nucleosomes being the first order of higher level structure. However, few data are reported on the efficiency of clustered-lesion processing within nucleosomal DNA templates. Here, we show retardation of cleavage of a single AP site by purified APE1 when contained in nucleosomal DNA, compared to cleavage of an AP site in non-nucleosomal DNA. This retardation seen in nucleosomal DNA was alleviated by incubation with CHO-K1 nuclear extract. When clustered DNA damage sites containing bistranded AP sites were present in nucleosomal DNA, efficient cleavage of the AP sites was observed after treatment with nuclear extract. The resultant DSB formation led to DNA dissociating from the histone core and nucleosomal dispersion. Clustered damaged sites containing bistranded AP site/8-oxoG residues showed no retardation of cleavage of the AP site but retardation of 8-oxoG excision, compared to isolated lesions, thus DSB formation was not seen. An increased understanding of processing of clustered DNA damage in a nucleosomal environment may lead to new strategies to enhance the cytotoxic effects of radiotherapeutics.

Indexed as

DNA CleavageDNA DamageAnimalsCell ExtractsCell NucleusCHO CellsCricetulusDNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesDNA RepairGuanineHumansNucleosomesTemplates, Genetic8-hydroxyguanineAPEX1 protein, humanCell ExtractsDNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesGuanineNucleosomesoxoguanine glycosylase 1, human8-oxoGAP siteBERClustered DNA damageNucleosome

Identifiers

PMID26439176
PMCPMC4655832
OpenAlexW1620406455

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.