Evidence map›Paper›PMID 36270581›Full record

ReviewJournal of molecular biology2022

Dynamics of the Artemis and DNA-PKcs Complex in the Repair of Double-Strand Breaks.

Go Watanabe, Michael R Lieber

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. DNA Repair Mechanisms.Methods in molecular biology (Clifton, N.J.) · 2027
    Review
  2. Review
  3. Review
  4. DNA Damage and Repair in Pancreatic Cancer-The Latest Findings.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Biomolecules · 2024
    Article
  12. Article
  13. Frontiers in cellular and infection microbiology · 2024
    Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. The flexible and iterative steps within the NHEJ pathway.Progress in biophysics and molecular biology
    Article
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

2 authors at 1 institution in 1 country.

Go WatanabeDepartment of Pathology, Department of Biochemistry & Molecular Biology, Department of Molecular Microbiology & Immunology, and Section of Molecular & Computational Biology, USC Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, 1441 Eastlake Ave, Rm. 5428, Los Angeles, CA 90089, USA.
Michael R LieberDepartment of Pathology, Department of Biochemistry & Molecular Biology, Department of Molecular Microbiology & Immunology, and Section of Molecular & Computational Biology, USC Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, 1441 Eastlake Ave, Rm. 5428, Los Angeles, CA 90089, USA. Electronic address: 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
Site-Specific Recombination in Human Health & DiseaseR35GM118009 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LIEBER, MICHAEL R · 2016 to 2025
$4.4M
NCI NIH HHS R01 CA100504NIGMS NIH HHS R35 GM118009
6 · The paper itself

Abstract

Pathologic chromosome breaks occur in human dividing cells ∼10 times per day, and physiologic breaks occur in each lymphoid cell many additional times per day. Nonhomologous DNA end joining (NHEJ) is the major pathway for the repair of all of these double-strand breaks (DSBs) during most of the cell cycle. Nearly all broken DNA ends require trimming before they can be suitable for joining by ligation. Artemis is the major nuclease for this purpose. Artemis is tightly regulated by one of the largest protein kinases, which tethers Artemis to its surface. This kinase is called DNA-dependent protein kinase catalytic subunit (or DNA-PKcs) because it is only active when it encounters a broken DNA end. With this activation, DNA-PKcs permits the Artemis catalytic domain to enter a large cavity in the center of DNA-PKcs. Given this remarkably tight supervision of Artemis by DNA-PKcs, it is an appropriate time to ask what we know about the Artemis:DNA-PKcs complex, as we integrate recent structural information with the biochemistry of the complex and how this relates to other NHEJ proteins and to V(D)J recombination in the immune system.

Indexed as

DNA-Activated Protein KinaseDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA End-Joining RepairEndonucleasesHumansNuclear ProteinsDCLRE1C protein, humanDNA-Activated Protein KinaseDNA-Binding ProteinsEndonucleasesNuclear Proteinscryo-EMDNA repairnonhomologous DNA end joining (NHEJ)severe combined immune deficiencyV(D)J recombination

Identifiers

PMID36270581
PMCPMC9940633
OpenAlexW4306757078

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.