Evidence map›Paper›PMID 33574136›Full record

ArticleGenome research2021

Enhancing CRISPR deletion via pharmacological delay of DNA-PKcs.

Núria Bosch-Guiteras, Tina Uroda, Hugo A Guillen-Ramirez, Rahel Riedo, Amiq Gazdhar, Roberta Esposito, Carlos Pulido-Quetglas, Yitzhak Zimmer, Michaela Medová, Rory Johnson

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Arrayed dual-gRNA CRISPR screening platform forMolecular therapy. Advances · 2026
    Article
  2. The aflatoxin BNAR cancer · 2025
    Article
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  7. Research progress of pathway and genome evolution in microbes.Synthetic and systems biotechnology · 2022
    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 2 institutions in 2 countries.

Núria Bosch-GuiterasDepartment of Medical Oncology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.ORCID 0000-0003-0331-0429
Tina Uroda *Department of Medical Oncology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Hugo A Guillen-Ramirez *Department of Medical Oncology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Rahel RiedoDepartment for BioMedical Research, University of Bern, 3008 Bern, Switzerland.
Amiq GazdharDepartment for BioMedical Research, University of Bern, 3008 Bern, Switzerland.
Roberta EspositoDepartment of Medical Oncology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Carlos Pulido-QuetglasDepartment of Medical Oncology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Yitzhak ZimmerDepartment for BioMedical Research, University of Bern, 3008 Bern, Switzerland.
Michaela MedováDepartment for BioMedical Research, University of Bern, 3008 Bern, Switzerland.
Rory JohnsonDepartment of Medical Oncology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.ORCID 0000-0003-4607-2782
University of Bern · CHUniversity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CRISPR-Cas9 deletion (CRISPR-del) is the leading approach for eliminating DNA from mammalian cells and underpins a variety of genome-editing applications. Target DNA, defined by a pair of double-strand breaks (DSBs), is removed during nonhomologous end-joining (NHEJ). However, the low efficiency of CRISPR-del results in laborious experiments and false-negative results. By using an endogenous reporter system, we show that repression of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs)-an early step in NHEJ-yields substantial increases in DNA deletion. This is observed across diverse cell lines, gene delivery methods, commercial inhibitors, and guide RNAs, including those that otherwise display negligible activity. We further show that DNA-PKcs inhibition can be used to boost the sensitivity of pooled functional screens and detect true-positive hits that would otherwise be overlooked. Thus, delaying the kinetics of NHEJ relative to DSB formation is a simple and effective means of enhancing CRISPR-deletion.

Indexed as

DNA Breaks, Double-StrandedGene EditingSequence DeletionAnimalsCRISPR-Cas SystemsDNADNA-Activated Protein KinaseDNA-Binding ProteinsDNA End-Joining RepairDNADNA-Activated Protein KinaseDNA-Binding Proteins

Identifiers

PMID33574136
PMCPMC7919447
OpenAlexW3126333601

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.