Evidence map›Paper›PMID 21945337›Full record

ArticleJournal of theoretical biology2012

Optimality in DNA repair.

Morgiane Richard, Matthew Fryett, Samantha Miller, Ian Booth, Celso Grebogi, Alessandro Moura

Open access · hybridAbstract read
In one paragraph

Article in Journal of theoretical biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Host methylglyoxal activates theProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
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

6 authors at 1 institution in 1 country.

Morgiane RichardInstitute of Complex Systems and Mathematical Biology, King's College, University of Aberdeen, Aberdeen, UK.
Matthew Fryett
Samantha Miller
Ian Booth
Celso Grebogi
Alessandro Moura
University of Aberdeen · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F003455/1Biotechnology and Biological Sciences Research Council BB/G010722
6 · The paper itself

Abstract

DNA within cells is subject to damage from various sources. Organisms have evolved a number of mechanisms to repair DNA damage. The activity of repair enzymes carries its own risk, however, because the repair of two nearby lesions may lead to the breakup of DNA and result in cell death. We propose a mathematical theory of the damage and repair process in the important scenario where lesions are caused in bursts. We use this model to show that there is an optimum level of repair enzymes within cells which optimises the cell's response to damage. This optimal level is explained as the best trade-off between fast repair and a low probability of causing double-stranded breaks. We derive our results analytically and test them using stochastic simulations, and compare our predictions with current biological knowledge.

Indexed as

Models, GeneticAnimalsCell DeathCell SurvivalDNA DamageDNA RepairDNA Repair EnzymesStochastic ProcessesDNA Repair Enzymes

Identifiers

PMID21945337
PMCPMC4071444
OpenAlexW2105223902

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.