ReviewMutation research2016
Risky business: Microhomology-mediated end joining.
Review in Mutation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed.
- CRISPR/Cas9 generated DSB clusters mimic complex lesions induced by high-LET radiation and shift repair from c-NHEJ to mutagenic repair pathways.Scientific reports · 2025Article
- Off-target effects in CRISPR-Cas genome editing for human therapeutics: Progress and challenges.Molecular therapy. Nucleic acids · 2025Review
- Comparative analysis of multiple DNA double-strand break repair pathways in CRISPR-mediated endogenous tagging.Communications biology · 2025Article
- Molecular mechanisms of extrachromosomal circular DNA formation.Nucleic acids research · 2025Review
- Dynamic interplay of cNHEJ and MMEJ pathways of DNA double-strand break repair during embryonic development in zebrafish.Scientific reports · 2025Article
- Structural and Mechanistic Diversity of Constitutional Chromoanagenesis.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Gene therapy for CNS disorders: modalities, delivery and translational challenges.Nature reviews. Neuroscience · 2024Review
- Unravelling the molecular basis of PARP inhibitor resistance in prostate cancer with homologous recombination repair deficiency.International review of cell and molecular biology · 2024Review
- Advances in Recombinant Adeno-Associated Virus Vectors for Neurodegenerative Diseases.Biomedicines · 2023Review
- Proper RPA acetylation promotes accurate DNA replication and repair.Nucleic acids research · 2023Article
- The remodeling of Z-DNA in the mammalian germ line.Biochemical Society transactions · 2022Article
- Clinical Landscape of PARP Inhibitors in Ovarian Cancer: Molecular Mechanisms and Clues to Overcome Resistance.Cancers · 2022Review
- Detection and characterization of genome-wide mutations in M1 vegetative cells of gamma-irradiated Arabidopsis.PLoS genetics · 2022Article
- Advance trends in targeting homology-directed repair for accurate gene editing: An inclusive review of small molecules and modified CRISPR-Cas9 systems.BioImpacts : BI · 2022Review
- MicroDNA levels are dependent on MMEJ, repressed by c-NHEJ pathway, and stimulated by DNA damage.Nucleic acids research · 2021Article
- Review
- Rtt105 promotes high-fidelity DNA replication and repair by regulating the single-stranded DNA-binding factor RPA.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Nanopore Sequencing Indicates That Tandem Amplification of Chromosome 20q11.21 in Human Pluripotent Stem Cells Is Driven by Break-Induced Replication.Stem cells and development · 2021Article
- Germline Structural Variations in Cancer Predisposition Genes.Frontiers in genetics · 2021Review
- Microhomology-Mediated Nonhomologous End Joining Caused Rearrangement ofFrontiers in genetics · 2021Article
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.
Funding
Abstract
Prevalence of microhomology (MH) at the breakpoint junctions in somatic and germ-line chromosomal rearrangements and in the programmed immune receptor rearrangements from cells deficient in classical end joining reveals an enigmatic process called MH-mediated end joining (MMEJ). MMEJ repairs DNA double strand breaks (DSBs) by annealing flanking MH and deleting genetic information at the repair junctions from yeast to humans. Being genetically distinct from canonical DNA DSB pathways, MMEJ is involved with the fusions of eroded/uncapped telomeres as well as with the assembly of chromosome fragments in chromothripsis. In this review article, we will discuss an up-to-date model representing the MMEJ process and the mechanism by which cells regulate MMEJ to limit repair-associated mutagenesis. We will also describe the possible therapeutic gains resulting from the inhibition of MMEJ in recombination deficient cancers. Lastly, we will embark on two contentious issues associated with MMEJ such as the significance of MH at the repair junction to be the hallmark of MMEJ and the relationship of MMEJ to other mechanistically related DSB repair pathways.
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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.