ArticleThe EMBO journal2017
Mutational signatures of non-homologous and polymerase theta-mediated end-joining in embryonic stem cells.
Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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.
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.
Who cites it
98 citing papers in PubMed, 149 citations in OpenAlex.
- DNA polymerase theta (Polθ): a novel candidate for targeted cancer therapy.Cancer biology & therapy · 2026Review
- The polymerase milieu of human papillomavirus.Journal of virology · 2026Review
- Disruption of microhomology-mediated end joining in Ewing sarcoma.Molecular cell · 2026Article
- Sam68 stimulates polymerase theta-mediated end-joining by suppressing poison exon inclusion in Polq mRNA.Nucleic acids research · 2026Article
- In vivo systematic detection of the outcomes of CRISPR-Cas9-mediated DNA repair in skeletal muscle stem cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- A mutational scar-based genome-wide map of DNA double-strand break repair.Nature communications · 2026Article
- Optimizing CRISPR precision in mouse embryos via microhomology-mediated end joining-dominant targeting.Communications biology · 2026Article
- POLQ-driven repair scars shape the immunogenic landscape of homologous recombination-deficient pancreatic cancer.bioRxiv : the preprint server for biology · 2026Article
- DNA Polymerase θ Drives Colorectal Cancer Progression through Wnt/β-Catenin Activation and Shows Potential Association with Immunosuppressive Microenvironment Remodeling.Oncology research · 2026Article
- Dynamic Assemblies in Genome Maintenance.Advances in experimental medicine and biology · 2026Review
- Polymerase theta repairs persistent G1-induced DNA breaks in S-phase during class switch recombination.Nature communications · 2025Article
- Megabase-scale loss of heterozygosity provoked by CRISPR-Cas9 DNA double-strand breaks.Molecular cell · 2025Article
- Disruption of Microhomology-mediated End-joining in Ewing Sarcoma.bioRxiv : the preprint server for biology · 2025Article
- Refined DNA repair manipulation enables a universal knock-in strategy in mouse embryos.Nature communications · 2025Article
- A non-tethering role for the Drosophila Pol θ linker domain in promoting damage resolution.Nucleic acids research · 2025Article
- The Evolutionary Potential of Chromoanagenesis.Methods in molecular biology (Clifton, N.J.) · 2025Article
- The interplay of DNA repair context with target sequence predictably biases Cas9-generated mutations.Nature communications · 2024Article
- Microhomology-Mediated End-Joining Chronicles: Tracing the Evolutionary Footprints of Genome Protection.Annual review of cell and developmental biology · 2024Review
- The interplay of DNA repair context with target sequence predictably biases Cas9-generated mutations.bioRxiv : the preprint server for biology · 2024Article
- Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells employ potentially mutagenic DNA repair mechanisms to avoid the detrimental effects of chromosome breaks on cell survival. While classical non-homologous end-joining (cNHEJ) is largely error-free, alternative end-joining pathways have been described that are intrinsically mutagenic. Which end-joining mechanisms operate in germ and embryonic cells and thus contribute to heritable mutations found in congenital diseases is, however, still largely elusive. Here, we determined the genetic requirements for the repair of CRISPR/Cas9-induced chromosomal breaks of different configurations, and establish the mutational consequences. We find that cNHEJ and polymerase theta-mediated end-joining (TMEJ) act both parallel and redundant in mouse embryonic stem cells and account for virtually all end-joining activity. Surprisingly, mutagenic repair by polymerase theta (Pol θ, encoded by the
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.