Evidence map›Paper›PMID 33672015›Full record

ArticleBiomolecules2021

A Targeted and Tuneable DNA Damage Tool Using CRISPR/Cas9.

Ioannis Emmanouilidis, Natalia Fili, Alexander W Cook, Yukti Hari-Gupta, Ália Dos Santos, Lin Wang, Marisa L Martin-Fernandez, Peter J I Ellis, Christopher P Toseland

Abstract read
In one paragraph

Article in Biomolecules, 2021. 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
–field-weighted citation impact
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.

  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

9 authors.

Ioannis EmmanouilidisSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.
Natalia FiliDepartment of Oncology and Metabolism, University of Sheffield, Sheffield S10 2RX, UK.ORCID 0000-0002-0898-0766
Alexander W CookDepartment of Oncology and Metabolism, University of Sheffield, Sheffield S10 2RX, UK.
Yukti Hari-GuptaSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.ORCID 0000-0002-8685-2153
Ália Dos SantosDepartment of Oncology and Metabolism, University of Sheffield, Sheffield S10 2RX, UK.
Lin WangCentral Laser Facility, Research Complex at Harwell, Science and Technology Facilities Council, Rutherford Appleton Laboratory, Harwell, Didcot, Oxford OX11 0QX, UK.ORCID 0000-0001-9141-5217
Marisa L Martin-FernandezCentral Laser Facility, Research Complex at Harwell, Science and Technology Facilities Council, Rutherford Appleton Laboratory, Harwell, Didcot, Oxford OX11 0QX, UK.ORCID 0000-0001-5496-6300
Peter J I EllisSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.ORCID 0000-0001-9709-7934
Christopher P ToselandDepartment of Oncology and Metabolism, University of Sheffield, Sheffield S10 2RX, UK.ORCID 0000-0002-1641-7535

Funding

Central Laser Facility, Science and Technology Facilities Council 19130001Medical Research Council MC_EX_MR/K015591/1Medical Research Council MR/M020606/1
6 · The paper itself

Abstract

Mammalian cells are constantly subjected to a variety of DNA damaging events that lead to the activation of DNA repair pathways. Understanding the molecular mechanisms of the DNA damage response allows the development of therapeutics which target elements of these pathways. Double-strand breaks (DSB) are particularly deleterious to cell viability and genome stability. Typically, DSB repair is studied using DNA damaging agents such as ionising irradiation or genotoxic drugs. These induce random lesions at non-predictive genome sites, where damage dosage is difficult to control. Such interventions are unsuitable for studying how different DNA damage recognition and repair pathways are invoked at specific DSB sites in relation to the local chromatin state. The RNA-guided Cas9 (CRISPR-associated protein 9) endonuclease enzyme is a powerful tool to mediate targeted genome alterations. Cas9-based genomic intervention is attained through DSB formation in the genomic area of interest. Here, we have harnessed the power to induce DSBs at defined quantities and locations across the human genome, using custom-designed promiscuous guide RNAs, based on in silico predictions. This was achieved using electroporation of recombinant Cas9-guide complex, which provides a generic, low-cost and rapid methodology for inducing controlled DNA damage in cell culture models.

Indexed as

CRISPR-Cas SystemsDNA Breaks, Double-StrandedDNA DamageCell SurvivalCisplatinComputer SimulationDNA RepairElectroporationEndonucleasesEscherichia coliGene EditingGenome, HumanGenomic InstabilityGenomicsHumansMicroscopy, ConfocalCisplatinEndonucleasesMutagensRNA, Guide, CRISPR-Cas SystemsCas9DNA damageDNA repairdouble-strand break

Identifiers

PMID33672015
PMCPMC7919286

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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.