Evidence map›Paper›PMID 32589683›Full record

ArticlePloS one2020

Participation of TDP1 in the repair of formaldehyde-induced DNA-protein cross-links in chicken DT40 cells.

Toshiaki Nakano, Mahmoud I Shoulkamy, Masataka Tsuda, Hiroyuki Sasanuma, Kouji Hirota, Minoru Takata, Shin-Ichiro Masunaga, Shunichi Takeda, Hiroshi Ide, Tadayoshi Bessho and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. 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

11 authors at 4 institutions in 2 countries.

Toshiaki NakanoDNA Damage Chemistry Research Group, Institute for Quantum Life Science, Kansai Photon Science Institute, National Institutes of Quantum and Radiological Science and Technology, Kizugawa, Kyoto, Japan.
Mahmoud I ShoulkamyDepartment of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Higashi-Hiroshima, Japan.ORCID 0000-0002-4736-1212
Masataka TsudaDepartment of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Higashi-Hiroshima, Japan.
Hiroyuki SasanumaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kouji HirotaDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Hachioji, Tokyo, Japan.
Minoru TakataDepartment of Late Effects Studies, Radiation Biology Center, Kyoto University, Kyoto, Japan.
Shin-Ichiro MasunagaDivision of Radiation Life Science, Institute for Integrated Radiation and Nuclear Science, Kyoto University, Kumatori, Osaka, Japan.
Shunichi TakedaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hiroshi IdeDepartment of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Higashi-Hiroshima, Japan.
Tadayoshi BesshoThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Keizo TanoDivision of Radiation Life Science, Institute for Integrated Radiation and Nuclear Science, Kyoto University, Kumatori, Osaka, Japan.ORCID 0000-0003-3900-0035
Kyoto University · JPHiroshima University · JPTokyo Metropolitan University · JPUniversity of Nebraska Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteins are covalently trapped on DNA to form DNA-protein cross-links (DPCs) when cells are exposed to DNA-damaging agents. Aldehyde compounds produce common types of DPCs that contain proteins in an undisrupted DNA strand. Tyrosyl-DNA phosphodiesterase 1 (TDP1) repairs topoisomerase 1 (TOPO1) that is trapped at the 3'-end of DNA. In the present study, we examined the contribution of TDP1 to the repair of formaldehyde-induced DPCs using a reverse genetic strategy with chicken DT40 cells. The results obtained showed that cells deficient in TDP1 were sensitive to formaldehyde. The removal of formaldehyde-induced DPCs was slower in tdp1-deficient cells than in wild type cells. We also found that formaldehyde did not produce trapped TOPO1, indicating that trapped TOPO1 was not a primary cytotoxic DNA lesion that was generated by formaldehyde and repaired by TDP1. The formaldehyde treatment resulted in the accumulation of chromosomal breakages that were more prominent in tdp1-deficient cells than in wild type cells. Therefore, TDP1 plays a critical role in the repair of formaldehyde-induced DPCs that are distinct from trapped TOPO1.

Indexed as

DNA RepairAnimalsCell LineChickensChromosome BreakageDecitabineDNADNA BreaksDNA Breaks, Double-StrandedDNA Topoisomerases, Type IFormaldehydeMitomycinPhosphoric Diester HydrolasesDecitabineDNADNA Topoisomerases, Type IFormaldehydeMitomycinPhosphoric Diester Hydrolases

Identifiers

PMID32589683
PMCPMC7319324
OpenAlexW3037044933

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.