Evidence map›Paper›PMID 25474029›Full record

ArticleNature protocols2015

A rapid, comprehensive system for assaying DNA repair activity and cytotoxic effects of DNA-damaging reagents.

Nan Jia, Yuka Nakazawa, Chaowan Guo, Mayuko Shimada, Mieran Sethi, Yoshito Takahashi, Hiroshi Ueda, Yuji Nagayama, Tomoo Ogi

Abstract read
PubMed Publisher
In one paragraph

Article in Nature protocols, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-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

30 citing papers in PubMed, 49 citations in OpenAlex.

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  18. A novel nonsense mutation ofHuman genome variation · 2020
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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

9 authors at 2 institutions in 2 countries.

Nan Jia1] Department of Pharmacology and Therapeutic Innovation, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. [2] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki University, Nagasaki, Japan. [3] Department of Molecular Medicine, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Yuka Nakazawa1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki University, Nagasaki, Japan. [2] Department of Molecular Medicine, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Chaowan Guo1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki University, Nagasaki, Japan. [2] Department of Molecular Medicine, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Mayuko Shimada1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki University, Nagasaki, Japan. [2] Department of Molecular Medicine, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Mieran SethiSt. John's Institute of Dermatology, Guy's and St. Thomas' Hospital, London, UK.
Yoshito TakahashiInnovative Beauty Science Laboratory, Kanebo Cosmetics Inc., Odawara, Japan.
Hiroshi UedaDepartment of Pharmacology and Therapeutic Innovation, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Yuji NagayamaDepartment of Molecular Medicine, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Tomoo Ogi1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki University, Nagasaki, Japan. [2] Department of Molecular Medicine, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan. [3] Microbial Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics, Mishima, Japan.
Nagasaki University · JPSt Thomas' Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA repair systems protect cells from genomic instability and carcinogenesis. Therefore, assays for measuring DNA repair activity are valuable, not only for clinical diagnoses of DNA repair deficiency disorders but also for basic research and anticancer drug development. Two commonly used assays are UDS (unscheduled DNA synthesis, requiring a precise measurement of an extremely small amount of repair DNA synthesis) and RRS (recovery of RNA synthesis after DNA damage). Both UDS and RRS are major endpoints for assessing the activity of nucleotide excision repair (NER), the most versatile DNA repair process. Conventional UDS and RRS assays are laborious and time-consuming, as they measure the incorporation of radiolabeled nucleosides associated with NER. Here we describe a comprehensive protocol for monitoring nonradioactive UDS and RRS by studying the incorporation of alkyne-conjugated nucleoside analogs followed by a fluorescent azide-coupling click-chemistry reaction. The system is also suitable for quick measurement of cell sensitivity to DNA-damaging reagents and for lentivirus-based complementation assays, which can be used to systematically determine the pathogenic genes associated with DNA repair deficiency disorders. A typical UDS or RRS assay using primary fibroblasts, including a virus complementation test, takes 1 week to complete.

Indexed as

AlkynesAzidesBiological AssayClick ChemistryDNADNA RepairFluorescenceGenetic Complementation TestHumansLentivirusNucleosidesRNAScintillation CountingUltraviolet RaysAlkynesAzidesDNANucleosidesRNA

Identifiers

PMID25474029
OpenAlexW2007991485

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.