Evidence map›Paper›PMID 39125869›Full record

ReviewInternational journal of molecular sciences2024

Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein.

David K Orren, Amrita Machwe

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Review
  2. Comprehensive genomics and functional analyses identifyTranslational cancer research · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. PLK1 phosphorylates WRN at replication forks.The Journal of pharmacology and experimental therapeutics · 2025
    Article
  14. 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

2 authors.

David K OrrenDepartment of Toxicology and Cancer Biology, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Amrita MachweDepartment of Toxicology and Cancer Biology, University of Kentucky College of Medicine, Lexington, KY 40536, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Werner syndrome (WS) is an autosomal recessive disease caused by loss of function of WRN. WS is a segmental progeroid disease and shows early onset or increased frequency of many characteristics of normal aging. WRN possesses helicase, annealing, strand exchange, and exonuclease activities and acts on a variety of DNA substrates, even complex replication and recombination intermediates. Here, we review the genetics, biochemistry, and probably physiological functions of the WRN protein. Although its precise role is unclear, evidence suggests WRN plays a role in pathways that respond to replication stress and maintain genome stability particularly in telomeric regions.

Indexed as

DNA ReplicationGenomic InstabilityWerner SyndromeWerner Syndrome HelicaseAnimalsHumansTelomereWerner Syndrome HelicaseWRN protein, humanDNA repairgenome instabilityhomologous recombinationRecQ helicasesreplication stresstelomere maintenanceWerner syndrome

Identifiers

PMID39125869
PMCPMC11311767

What OpenQuestion holds

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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.