Evidence map›Paper›PMID 20192759›Full record

ReviewAnnual review of biochemistry2010

The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway.

Michael R Lieber

Open access · greenAbstract readReview
In one paragraph

Review in Annual review of biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,542 papers.

0numbers the graph read from it
0cells of the map it votes in
1,542citing papers in PubMed
62.2field-weighted citation impact, top 1% of its field
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

1,542 citing papers in PubMed, 2,798 citations in OpenAlex.

  1. Article
  2. Article
  3. Sensitizing carbapenem-resistant Klebsiella pneumoniae using a compact Cascade-Cas3 system.International microbiology : the official journal of the Spanish Society for Microbiology · 2026
    Article
  4. Core NHEJ Factors Maintain Synapsis Across Diverse DNA End Structures.bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Metabolic engineering ofApplied and environmental microbiology · 2026
    Review
  9. Review
  10. Treatment of Huntington's disease with a pan-HTT-targeting CRISPR nuclease.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  11. Article
  12. Frameshift Mutations in Exon 1 ofJournal of developmental biology · 2026
    Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

1,482 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Michael R LieberNorris Comprehensive Cancer Center, Department of Pathology, University of Southern California Keck School of Medicine, Los Angeles, California 90089, USA. lieber@usc.edu
University of Southern California · US

Funding

MECHANISM AND REGULATION OF NONHOMOLOGOUS DNA ENDJOININGR01CA100504 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LIEBER, MICHAEL R · 2003 to 2021
$5.0M
NCI NIH HHS R01 CA100504
6 · The paper itself

Abstract

Double-strand DNA breaks are common events in eukaryotic cells, and there are two major pathways for repairing them: homologous recombination (HR) and nonhomologous DNA end joining (NHEJ). The various causes of double-strand breaks (DSBs) result in a diverse chemistry of DNA ends that must be repaired. Across NHEJ evolution, the enzymes of the NHEJ pathway exhibit a remarkable degree of structural tolerance in the range of DNA end substrate configurations upon which they can act. In vertebrate cells, the nuclease, DNA polymerases, and ligase of NHEJ are the most mechanistically flexible and multifunctional enzymes in each of their classes. Unlike repair pathways for more defined lesions, NHEJ repair enzymes act iteratively, act in any order, and can function independently of one another at each of the two DNA ends being joined. NHEJ is critical not only for the repair of pathologic DSBs as in chromosomal translocations, but also for the repair of physiologic DSBs created during variable (diversity) joining [V(D)J] recombination and class switch recombination (CSR). Therefore, patients lacking normal NHEJ are not only sensitive to ionizing radiation (IR), but also severely immunodeficient.

Indexed as

DNA Breaks, Double-StrandedDNA RepairAnimalsDeoxyribonucleasesDNA-Directed DNA PolymeraseDNA LigasesHumansDeoxyribonucleasesDNA-Directed DNA PolymeraseDNA Ligases

Identifiers

PMID20192759
PMCPMC3079308
OpenAlexW2164995160

What OpenQuestion holds

Textmetadata
LicenceTDM
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.