Evidence map›Paper›PMID 30030458›Full record

ArticleScientific reports2018

Assessment of DNA-PKcs kinase activity by quantum dot-based microarray.

Florian Lafont, Nizar Ayadi, Cathy Charlier, Pierre Weigel, Igor Nabiev, Houda Benhelli-Mokrani, Fabrice Fleury

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. 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
0.3field-weighted citation impact, top 43% 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, 4 citations in OpenAlex.

  1. Article
  2. 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

7 authors at 2 institutions in 2 countries.

Florian LafontGroup of Mechanism and Regulation of DNA Repair and IMPACT platform, UFIP UMR CNRS 6286/University of Nantes, 44322, Nantes, France.ORCID 0000-0002-9240-7806
Nizar AyadiGroup of Mechanism and Regulation of DNA Repair and IMPACT platform, UFIP UMR CNRS 6286/University of Nantes, 44322, Nantes, France.
Cathy CharlierGroup of Mechanism and Regulation of DNA Repair and IMPACT platform, UFIP UMR CNRS 6286/University of Nantes, 44322, Nantes, France.
Pierre WeigelGroup of Mechanism and Regulation of DNA Repair and IMPACT platform, UFIP UMR CNRS 6286/University of Nantes, 44322, Nantes, France.
Igor NabievLaboratoire de Recherche en Nanosciences, LRN-EA4682, UFR de Pharmacie, Université de Reims Champagne-Ardenne, 51100, Reims, France.ORCID 0000-0002-8391-040X
Houda Benhelli-MokraniGroup of Mechanism and Regulation of DNA Repair and IMPACT platform, UFIP UMR CNRS 6286/University of Nantes, 44322, Nantes, France.
Fabrice FleuryGroup of Mechanism and Regulation of DNA Repair and IMPACT platform, UFIP UMR CNRS 6286/University of Nantes, 44322, Nantes, France. fleury-f@univ-nantes.fr.
Centre National de la Recherche Scientifique · FRNational Research Nuclear University MEPhI · RU

Funding

Ligue Contre le Cancer Comité 44 et 85Russian Science Foundation (RSF) 17-15-01533
6 · The paper itself

Abstract

Therapeutic efficacy against cancer is often based on a variety of DNA lesions, including DNA double-strand breaks (DSBs) which are repaired by homologous recombination and non-homologous end joining (NHEJ) pathways. In the past decade, the functions of the DNA repair proteins have been described as a potential mechanism of resistance in tumor cells. Therefore, the DNA repair proteins have become targets to improve the efficacy of anticancer therapy. Given the central role of DNA-PKcs in NHEJ, the therapeutic efficacy of targeting DNA-PKcs is frequently described as a strategy to prevent repair of treatment-induced DNA damage in cancer cells. The screening of a new inhibitor acting as a sensitizer requires the development of a high-throughput tool in order to identify and assess the most effective molecule. Here, we describe the elaboration of an antibody microarray dedicated to the NHEJ pathway that we used to evaluate the DNA-PKcs kinase activity in response to DNA damage. By combining a protein microarray with Quantum-Dot detection, we show that it is possible to follow the modification of phosphoproteomic cellular profiles induced by inhibitors during the response to DNA damage. Finally, we discuss the promising tool for screening kinase inhibitors and targeting DSB repair to improve cancer treatment.

Indexed as

DNA End-Joining RepairAntibodiesAntineoplastic AgentsDNA-Activated Protein KinaseDNA Breaks, Double-StrandedDNA RepairMicroarray AnalysisNeoplasmsNuclear ProteinsProtein Kinase InhibitorsQuantum DotsAntibodiesAntineoplastic AgentsDNA-Activated Protein KinaseNuclear ProteinsPRKDC protein, humanProtein Kinase Inhibitors

Identifiers

PMID30030458
PMCPMC6054677
OpenAlexW2883784851

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.