Evidence map›Paper›PMID 34463774›Full record

ReviewCellular and molecular life sciences : CMLS2021

DNA damage responses that enhance resilience to replication stress.

Kazumasa Yoshida, Masatoshi Fujita

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Piperazine derivatives as anticancer agents: a medicinal chemistry review of structure, mechanism, and clinical translation.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  2. Article
  3. Article
  4. Wdr5-mediated H3K4 methylation facilitates HSPC development via maintenance of genomic stability in zebrafish.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Inflammation: A New Look at an Old Problem.International journal of molecular sciences · 2022
    Review
  12. The partner-swapping sliding clamp loader exposed.Nature structural & molecular biology · 2022
    Article
  13. Heat Shock Protein 90 as Therapeutic Target for CVDs and Heart Ageing.International journal of molecular sciences · 2022
    Review
  14. Review
  15. 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.

Kazumasa YoshidaDepartment of Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Masatoshi FujitaDepartment of Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan. mfujita@phar.kyushu-u.ac.jp.ORCID http://orcid.org/0000-0001-6617-2452
Kyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During duplication of the genome, eukaryotic cells may experience various exogenous and endogenous replication stresses that impede progression of DNA replication along chromosomes. Chemical alterations in template DNA, imbalances of deoxynucleotide pools, repetitive sequences, tight DNA-protein complexes, and conflict with transcription can negatively affect the replication machineries. If not properly resolved, stalled replication forks can cause chromosome breaks leading to genomic instability and tumor development. Replication stress is enhanced in cancer cells due, for example, to the loss of DNA repair genes or replication-transcription conflict caused by activation of oncogenic pathways. To prevent these serious consequences, cells are equipped with diverse mechanisms that enhance the resilience of replication machineries to replication stresses. This review describes DNA damage responses activated at stressed replication forks and summarizes current knowledge on the pathways that promote faithful chromosome replication and protect chromosome integrity, including ATR-dependent replication checkpoint signaling, DNA cross-link repair, and SLX4-mediated responses to tight DNA-protein complexes that act as barriers. This review also focuses on the relevance of replication stress responses to selective cancer chemotherapies.

Indexed as

AnimalsChromosomesDNADNA DamageDNA RepairDNA ReplicationHumansProteinsDNAProteinsCMG helicaseDNA polymeraseFanconi anemiaGenome maintenanceReplication fork arrest

Identifiers

PMID34463774
PMCPMC11072782
OpenAlexW3196485964

What OpenQuestion holds

Textmetadata
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.