Evidence map›Paper›PMID 34718749›Full record

ArticleNucleic acids research2021

Timely termination of repair DNA synthesis by ATAD5 is important in oxidative DNA damage-induced single-strand break repair.

Su Hyung Park, Youyoung Kim, Jae Sun Ra, Min Woo Wie, Mi-Sun Kang, Sukhyun Kang, Kyungjae Myung, Kyoo-Young Lee

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. ATAD5 functions as a regulatory platform for Ub-PCNA deubiquitination.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Nanoscale Interaction of Endonuclease APE1 with DNA.International journal of molecular sciences · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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  19. Review
  20. 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

8 authors at 1 institution in 1 country.

Su Hyung ParkCenter for Genomic Integrity, Institute for Basic Science (IBS), Ulsan 44919, Republic of Korea.
Youyoung KimCenter for Genomic Integrity, Institute for Basic Science (IBS), Ulsan 44919, Republic of Korea.
Jae Sun RaCenter for Genomic Integrity, Institute for Basic Science (IBS), Ulsan 44919, Republic of Korea.
Min Woo WieCenter for Genomic Integrity, Institute for Basic Science (IBS), Ulsan 44919, Republic of Korea.
Mi-Sun KangCenter for Genomic Integrity, Institute for Basic Science (IBS), Ulsan 44919, Republic of Korea.
Sukhyun KangCenter for Genomic Integrity, Institute for Basic Science (IBS), Ulsan 44919, Republic of Korea.
Kyungjae MyungCenter for Genomic Integrity, Institute for Basic Science (IBS), Ulsan 44919, Republic of Korea.
Kyoo-Young LeeCenter for Genomic Integrity, Institute for Basic Science (IBS), Ulsan 44919, Republic of Korea.ORCID 0000-0003-2433-0226
Institute for Basic Science · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species (ROS) generate oxidized bases and single-strand breaks (SSBs), which are fixed by base excision repair (BER) and SSB repair (SSBR), respectively. Although excision and repair of damaged bases have been extensively studied, the function of the sliding clamp, proliferating cell nuclear antigen (PCNA), including loading/unloading, remains unclear. We report that, in addition to PCNA loading by replication factor complex C (RFC), timely PCNA unloading by the ATPase family AAA domain-containing protein 5 (ATAD5)-RFC-like complex is important for the repair of ROS-induced SSBs. We found that PCNA was loaded at hydrogen peroxide (H2O2)-generated direct SSBs after the 3'-terminus was converted to the hydroxyl moiety by end-processing enzymes. However, PCNA loading rarely occurred during BER of oxidized or alkylated bases. ATAD5-depleted cells were sensitive to acute H2O2 treatment but not methyl methanesulfonate treatment. Unexpectedly, when PCNA remained on DNA as a result of ATAD5 depletion, H2O2-induced repair DNA synthesis increased in cancerous and normal cells. Based on higher H2O2-induced DNA breakage and SSBR protein enrichment by ATAD5 depletion, we propose that extended repair DNA synthesis increases the likelihood of DNA polymerase stalling, shown by increased PCNA monoubiquitination, and consequently, harmful nick structures are more frequent.

Indexed as

DNA End-Joining RepairDNA ReplicationATPases Associated with Diverse Cellular ActivitiesDNA-Binding ProteinsHEK293 CellsHeLa CellsHumansHydrogen PeroxideOxidative StressProliferating Cell Nuclear AntigenATAD5 protein, humanATPases Associated with Diverse Cellular ActivitiesDNA-Binding ProteinsHydrogen PeroxidePCNA protein, humanProliferating Cell Nuclear Antigen

Identifiers

PMID34718749
PMCPMC8599757
OpenAlexW3209109887

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.