ReviewSub-cellular biochemistry2010
Nonhomologous DNA end joining (NHEJ) and chromosomal translocations in humans.
Review in Sub-cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
What it found
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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
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- Successful birth after preimplantation genetic testing for a couple with two different reciprocal translocations and review of the literature.Reproductive biology and endocrinology : RB&E · 2021Pooled it
- Apoptosis-driven chromosomal rearrangements in cancer: CAD cleavage, nuclear architecture, and microhomology-mediated end joining.Oncogenesis · 2026Review
- Invas: an inversion-aware method for transcriptome assembly.Nature communications · 2026Article
- Dual roles of two Tfdps in germline nuclear meiosis and somatic nuclear fragmentation during sexual reproduction in the unicellular organismMarine life science & technology · 2026Article
- Emerging CRISPR Approaches for Countering Immune Evasion: Insight from Recent Studies.International journal of molecular sciences · 2026Review
- CRISPR/Cas9 a genomic engineering technology for treatment in ALS mouse models.Regenerative therapy · 2025Review
- Chromosomes remain individualized through interphase in embryos of the tardigradebioRxiv : the preprint server for biology · 2025Article
- Dynamic crosstalk between amino acid metabolism and cancer drug efficacy: From mechanisms to therapeutic opportunities.iScience · 2025Review
- Unlocking genetic potential: a review of the role of CRISPR/Cas technologies in rapeseed improvement.Stress biology · 2025Review
- Combining long-read DNA and RNA sequencing to enhance molecular understanding of structural variations leading to copy gains.Computational and structural biotechnology journal · 2025Article
- Article
- High-complexity of DNA double-strand breaks is key for alternative end-joining choice.Communications biology · 2024Article
- iMUT-seq: high-resolution DSB-induced mutation profiling reveals prevalent homologous-recombination dependent mutagenesis.Nature communications · 2023Article
- Specificity of cancer-related chromosomal translocations is linked to proximity after the DNA double-strand break and subsequent selection.NAR cancer · 2023Article
- Fold-back mechanism originating inv-dup-del rearrangements in chromosomes 13 and 15.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Article
- The remodeling of Z-DNA in the mammalian germ line.Biochemical Society transactions · 2022Article
- Recurrent Translocations in Topoisomerase Inhibitor-Related Leukemia Are Determined by the Features of DNA Breaks Rather Than by the Proximity of the Translocating Genes.International journal of molecular sciences · 2022Article
- The mechanisms of human lymphoid chromosomal translocations and their medical relevance.Critical reviews in biochemistry and molecular biology · 2022Article
- A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress.Scientific reports · 2022Article
- Functions of ADP-ribose transferases in the maintenance of telomere integrity.Cellular and molecular life sciences : CMLS · 2022Review
17 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
5 authors at 1 institution in 1 country.
Funding
Abstract
Double-strand breaks (DSBs) arise in dividing cells about ten times per cell per day. Causes include replication across a nick, free radicals of oxidative metabolism, ionizing radiation, and inadvertent action by enzymes of DNA metabolism (such as failures of type II topoisomerases or cleavage by recombinases at off-target sites). There are two major double-strand break repair pathways. Homologous recombination (HR) can repair double-strand breaks, but only during S phase and typically only if there are hundreds of base pairs of homology. The more commonly used pathway is nonhomologous DNA end joining, abbreviated NHEJ. NHEJ can repair a DSB at any time during the cell cycle and does not require any homology, although a few nucleotides of terminal microhomology are often utilized by the NHEJ enzymes, if present. The proteins and enzymes of NHEJ include Ku, DNA-PKcs, Artemis, DNA polymerase mu (Pol micro), DNA polymerase lambda (Pol lambda), XLF (also called Cernunnos), XRCC4, and DNA ligase IV. These enzymes constitute what some call the classical NHEJ pathway, and in wild type cells, the vast majority of joining events appear to proceed using these components. NHEJ is present in many prokaryotes, as well as all eukaryotes, and very similar mechanistic flexibility evolved both convergently and divergently. When two double-strand breaks occur on different chromosomes, then the rejoining is almost always done by NHEJ. The causes of DSBs in lymphomas most often involve the RAG or AID enzymes that function in the specialized processes of antigen receptor gene rearrangement.
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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.