Evidence map›Paper›PMID 25803306›Full record

ArticleNature biotechnology2015

Increasing the efficiency of homology-directed repair for CRISPR-Cas9-induced precise gene editing in mammalian cells.

Van Trung Chu, Timm Weber, Benedikt Wefers, Wolfgang Wurst, Sandrine Sander, Klaus Rajewsky, Ralf Kühn

Erratum issuedAbstract read
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In one paragraph

Article in Nature biotechnology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 696 papers.

0numbers the graph read from it
0cells of the map it votes in
696citing 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

696 citing papers in PubMed.

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  12. ALK Knock-In Reporter Reveals APE1 as a Negative Regulator ofInternational journal of molecular sciences · 2026
    Article
  13. CRISPR Gene Tagging for Illuminating Endogenous Protein Dynamics.International journal of molecular sciences · 2026
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. A modified CRISPR/Cas9 approach in silencing the triplication in Down syndrome: A treatment path XISTs.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  19. Article
  20. Article

636 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Van Trung ChuMax-Delbrück-Center for Molecular Medicine, Berlin, Germany.
Timm WeberMax-Delbrück-Center for Molecular Medicine, Berlin, Germany.
Benedikt Wefers1] Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. [2] Deutsches Zentrum für Neurodegenerative Erkrankungen e.V., Munich, Germany.ORCID 0000000224929389
Wolfgang Wurst1] Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. [2] Deutsches Zentrum für Neurodegenerative Erkrankungen e.V., Munich, Germany. [3] Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilians-Universität München, Munich, Germany.
Sandrine SanderMax-Delbrück-Center for Molecular Medicine, Berlin, Germany.
Klaus RajewskyMax-Delbrück-Center for Molecular Medicine, Berlin, Germany.
Ralf Kühn1] Max-Delbrück-Center for Molecular Medicine, Berlin, Germany. [2] Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. [3] Berlin Institute of Health, Berlin, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The insertion of precise genetic modifications by genome editing tools such as CRISPR-Cas9 is limited by the relatively low efficiency of homology-directed repair (HDR) compared with the higher efficiency of the nonhomologous end-joining (NHEJ) pathway. To enhance HDR, enabling the insertion of precise genetic modifications, we suppressed the NHEJ key molecules KU70, KU80 or DNA ligase IV by gene silencing, the ligase IV inhibitor SCR7 or the coexpression of adenovirus 4 E1B55K and E4orf6 proteins in a 'traffic light' and other reporter systems. Suppression of KU70 and DNA ligase IV promotes the efficiency of HDR 4-5-fold. When co-expressed with the Cas9 system, E1B55K and E4orf6 improved the efficiency of HDR up to eightfold and essentially abolished NHEJ activity in both human and mouse cell lines. Our findings provide useful tools to improve the frequency of precise gene modifications in mammalian cells.

Indexed as

AdenoviridaeAdenovirus E4 ProteinsAnimalsCell LineCRISPR-Cas SystemsDNA Breaks, Double-StrandedDNA End-Joining RepairDNA Ligase ATPDNA LigasesGene Expression RegulationGenetic EngineeringGenome, HumanHomologous RecombinationHumansMiceViral ProteinsAdenovirus E4 ProteinsDNA Ligase ATPDNA LigasesE1B55K protein, adenovirusE4orf6 protein, adenovirusLIG4 protein, humanViral Proteins

Identifiers

PMID25803306

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.