Evidence map›Paper›PMID 36028228›Full record

ReviewAnnual review of genetics2022

Genome Protection by DNA Polymerase θ.

Richard D Wood, Sylvie Doublié

Open access · bronzeAbstract readReview
In one paragraph

Review in Annual review of genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. The Pharmacologic Profile of ART6043, a First-in-Class Clinical DNA Polymerase Theta Polymerase Domain Inhibitor Potentiating PARP Inhibitor Efficacy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  3. Article
  4. Article
  5. Beyond Short Microhomologies: Mismatch-Compatible Pol θ-Mediated DNA Damage Repair.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  6. Review
  7. Coordinated transfer of DNA between Pol θ and Pol δ resets microhomology choice during double-strand break repair.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Review
  9. Article
  10. Making 3' ends meet.Nature structural & molecular biology · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. ISGylation: is our genome yearning for such a modification?Acta biochimica et biophysica Sinica · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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 2 institutions in 1 country.

Richard D WoodDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Center, Houston, Texas, USA; email: rwood@mdanderson.org.
Sylvie DoubliéDepartment of Microbiology and Molecular Genetics, University of Vermont, Burlington, Vermont, USA; email: sdoublie@uvm.edu.
The University of Texas MD Anderson Cancer Center · USUniversity of Vermont · US

Funding

Structural determinants of Pol theta functionP01CA247773 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DALE A RAMSDEN · 2020 to 2026
$15.2M
Project 4: Coordinating Nucleolytic Pathways During Crosslink RepairP01CA193124 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WOOD, RICHARD D · 2017 to 2022
$9.6M
Processing of Radiation Damage by Translesion DNA SynthesisR01CA052040 · NCI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI DOUBLIE, SYLVIE · 1991 to 2017
$4.5M
NCI NIH HHS P01 CA193124NCI NIH HHS P01 CA247773NCI NIH HHS R01 CA052040
6 · The paper itself

Abstract

DNA polymerase θ (Pol θ) is a DNA repair enzyme widely conserved in animals and plants. Pol θ uses short DNA sequence homologies to initiate repair of double-strand breaks by theta-mediated end joining. The DNA polymerase domain of Pol θ is at the C terminus and is connected to an N-terminal DNA helicase-like domain by a central linker. Pol θ is crucial for maintenance of damaged genomes during development, protects DNA against extensive deletions, and limits loss of heterozygosity. The cost of using Pol θ for genome protection is that a few nucleotides are usually deleted or added at the repair site. Inactivation of Pol θ often enhances the sensitivity of cells to DNA strand-breaking chemicals and radiation. Since some homologous recombination-defective cancers depend on Pol θ for growth, inhibitors of Pol θ may be useful in treating such tumors.

Indexed as

DNA-Directed DNA PolymeraseNeoplasmsAnimalsDNADNA DamageDNA End-Joining RepairDNA Polymerase thetaDNADNA-Directed DNA PolymeraseDNA Polymerase thetaDNA double-strand breaksDNA helicaseDNA polymerasesDNA repairmutationstranslesion DNA synthesis

Identifiers

PMID36028228
PMCPMC10351424
OpenAlexW4293440026

What Socratic 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 Socratic graph.