Evidence map›Paper›PMID 35194903›Full record

ArticleGenes to cells : devoted to molecular & cellular mechanisms2022

XRCC1 counteracts poly(ADP ribose)polymerase (PARP) poisons, olaparib and talazoparib, and a clinical alkylating agent, temozolomide, by promoting the removal of trapped PARP1 from broken DNA.

Kouji Hirota, Masato Ooka, Naoto Shimizu, Kousei Yamada, Masataka Tsuda, Mahmoud Abdelghany Ibrahim, Shintaro Yamada, Hiroyuki Sasanuma, Mitsuko Masutani, Shunichi Takeda

Open access · bronzeAbstract read
In one paragraph

Article in Genes to cells : devoted to molecular & cellular mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. PARP1 UFMylation ensures the stability of stalled replication forks.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  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

10 authors at 5 institutions in 3 countries.

Kouji HirotaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0000-0003-1676-979X
Masato OokaDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Tokyo, Japan.
Naoto ShimizuDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kousei YamadaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Masataka TsudaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Mahmoud Abdelghany IbrahimDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Shintaro YamadaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hiroyuki SasanumaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Mitsuko MasutaniDepartment of Molecular and Genomic Biomedicine, CBMM, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Shunichi TakedaShenzhen University School of Medicine, Shenzhen, Guangdong, China.
Kyoto University · JPHiroshima University · JPNagasaki University · JPNational Institutes of Health · USShenzhen University · CN

Funding

Japan Society for the Promotion of Science, Core-to-Core Program, A. Advanced Research Network KAKENHI JP16H01314Japan Society for the Promotion of Science, Core-to-Core Program, A. Advanced Research Network KAKENHI JP16H06306Japan Society for the Promotion of Science, Core-to-Core Program, A. Advanced Research Network KAKENHI JP16H12595Japan Society for the Promotion of Science, Core-to-Core Program, A. Advanced Research Network KAKENHI JP19KK0210Japan Society for the Promotion of Science, Core-to-Core Program, A. Advanced Research Network KAKENHI JP20H04337Takeda Pharmaceutical Company Takeda Science FoundationYamada Science Foundation
6 · The paper itself

Abstract

Base excision repair (BER) removes damaged bases by generating single-strand breaks (SSBs), gap-filling by DNA polymerase β (POLβ), and resealing SSBs. A base-damaging agent, methyl methanesulfonate (MMS) is widely used to study BER. BER increases cellular tolerance to MMS, anti-cancer base-damaging drugs, temozolomide, carmustine, and lomustine, and to clinical poly(ADP ribose)polymerase (PARP) poisons, olaparib and talazoparib. The poisons stabilize PARP1/SSB complexes, inhibiting access of BER factors to SSBs. PARP1 and XRCC1 collaboratively promote SSB resealing by recruiting POLβ to SSBs, but XRCC1

Indexed as

PoisonsPoly(ADP-ribose) PolymerasesAdenosine Diphosphate RiboseAlkylating AgentsDNADNA DamageDNA RepairMethyl MethanesulfonatePhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsTemozolomideAdenosine Diphosphate RiboseAlkylating AgentsDNAMethyl MethanesulfonateolaparibPhthalazinesPiperazinesPoisonsPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasestalazoparibTemozolomidecarmustinelomustineolaparibPARP1PARP poisontalazoparibtemozolomideXRCC1

Identifiers

PMID35194903
PMCPMC9310723
OpenAlexW4212884656

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.