Evidence map›Paper›PMID 26287260›Full record

ReviewBiomolecules2015

Genome Instability in Development and Aging: Insights from Nucleotide Excision Repair in Humans, Mice, and Worms.

Diletta Edifizi, Björn Schumacher

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Chromosomal instability and its effect on cell lines.Cancer reports (Hoboken, N.J.) · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Interleukin-6: Molecule in the Intersection of Cancer, Ageing and COVID-19.International journal of molecular sciences · 2020
    Review
  10. The role of poly(ADP-ribose) polymerases in manganese exposed Caenorhabditis elegans.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2020
    Article
  11. The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019
    Review
  12. Article
  13. Impact of DNA repair and stability defects on cortical development.Cellular and molecular life sciences : CMLS · 2018
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Diletta EdifiziInstitute for Genome Stability in Aging and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany. edifizid@uni-koeln.de.
Björn SchumacherInstitute for Genome Stability in Aging and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany. bjoern.schumacher@uni-koeln.de.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DE

Funding

European Research Council 260383
6 · The paper itself

Abstract

DNA damage causally contributes to aging and cancer. Congenital defects in nucleotide excision repair (NER) lead to distinct cancer-prone and premature aging syndromes. The genetics of NER mutations have provided important insights into the distinct consequences of genome instability. Recent work in mice and C. elegans has shed new light on the mechanisms through which developing and aging animals respond to persistent DNA damage. The various NER mouse mutants have served as important disease models for Xeroderma pigmentosum (XP), Cockayne syndrome (CS), and trichothiodystrophy (TTD), while the traceable genetics of C. elegans have allowed the mechanistic delineation of the distinct outcomes of genome instability in metazoan development and aging. Intriguingly, highly conserved longevity assurance mechanisms respond to transcription-blocking DNA lesions in mammals as well as in worms and counteract the detrimental consequences of persistent DNA damage. The insulin-like growth factor signaling (IIS) effector transcription factor DAF-16 could indeed overcome DNA damage-driven developmental growth delay and functional deterioration even when DNA damage persists. Longevity assurance mechanisms might thus delay DNA damage-driven aging by raising the threshold when accumulating DNA damage becomes detrimental for physiological tissue functioning.

Indexed as

Genomic InstabilityAgingAnimalsCaenorhabditis elegansDNA DamageDNA RepairHumansMiceagingCockayne syndrome (CS)DNA damageGlobal-genome nucleotide-excision repair (GG-NER)growth hormone/insulin-like growth factor 1 (GH/IGF1) signalinglongevityNucleotide-excision repair (NER)somatotropic axisTranscription-coupled nucleotide excision repair (TC-NER)Ultraviolet Light (UV)

Identifiers

PMID26287260
PMCPMC4598778
OpenAlexW1880666155

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.