Evidence map›Paper›PMID 28463453›Full record

ReviewJournal of cellular physiology2018

A simple answer to complex questions: Caenorhabditis elegans as an experimental model for examining the DNA damage response and disease genes.

Matthias Rieckher, Arturo Bujarrabal, Markus A Doll, Najmeh Soltanmohammadi, Björn Schumacher

Abstract readReview
In one paragraph

Review in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Biomolecules · 2024
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Frontiers in aging · 2022
    Review
  9. Article
  10. Review
  11. Article
  12. Xenobiotic metabolism and transport inJournal of toxicology and environmental health. Part B, Critical reviews · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. 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

5 authors at 1 institution in 1 country.

Matthias RieckherInstitute for Genome Stability in Ageing and Disease, Cologne Cluster of Excellence in Cellular Stress Responses in Aging-Associated Diseases (CECAD), and Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany.
Arturo BujarrabalInstitute for Genome Stability in Ageing and Disease, Cologne Cluster of Excellence in Cellular Stress Responses in Aging-Associated Diseases (CECAD), and Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany.
Markus A DollInstitute for Genome Stability in Ageing and Disease, Cologne Cluster of Excellence in Cellular Stress Responses in Aging-Associated Diseases (CECAD), and Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany.
Najmeh SoltanmohammadiInstitute for Genome Stability in Ageing and Disease, Cologne Cluster of Excellence in Cellular Stress Responses in Aging-Associated Diseases (CECAD), and Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany.
Björn SchumacherInstitute for Genome Stability in Ageing and Disease, Cologne Cluster of Excellence in Cellular Stress Responses in Aging-Associated Diseases (CECAD), and Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany.ORCID 0000-0001-6097-5238
University of Cologne · DE

Funding

European Research Council 260383
6 · The paper itself

Abstract

The genetic information is constantly challenged by genotoxic attacks. DNA repair mechanisms evolved early in evolution and recognize and remove the various lesions. A complex network of DNA damage responses (DDR) orchestrates a variety of physiological adaptations to the presence of genome instability. Erroneous repair or malfunctioning of the DDR causes cancer development and the accumulation of DNA lesions drives the aging process. For understanding the complex DNA repair and DDR mechanisms it is pivotal to employ simple metazoan as model systems. The nematode Caenorhabditis elegans has become a well-established and popular experimental organism that allows dissecting genome stability mechanisms in dynamic and differentiated tissues and under physiological conditions. We provide an overview of the distinct advantages of the nematode system for studying DDR and provide a range of currently applied methodologies.

Indexed as

Genes, HelminthModels, TheoreticalAnimalsBiological AssayCaenorhabditis elegansDiseaseDNA DamageDNA RepairagingC. elegansDNA damage responseDNA repairgenome stability

Identifiers

PMID28463453
PMCPMC5562273
OpenAlexW2610242636

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.