Evidence map›Paper›PMID 31410467›Full record

ReviewNucleic acids research2019

DNA polymerase ζ in DNA replication and repair.

Sara K Martin, Richard D Wood

Open access · goldAbstract readReview
In one paragraph

Review in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

64 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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  8. The 9-1-1 complex protects ssDNA gaps in BRCA2-deficient cancer.bioRxiv : the preprint server for biology · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. The Etiology of Moebius Syndrome-Making the Case for Animal Models.International journal of molecular sciences · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Patterns of spontaneous and induced genomic alterations inApplied and environmental microbiology · 2025
    Article
  18. Article
  19. Article
  20. Article

4 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

2 authors at 1 institution in 1 country.

Sara K MartinDepartment of Epigenetics & Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA and The University of Texas MD Anderson Cancer Center UT Health Graduate School of Biomedical Sciences.
Richard D WoodDepartment of Epigenetics & Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA and The University of Texas MD Anderson Cancer Center UT Health Graduate School of Biomedical Sciences.
The University of Texas MD Anderson Cancer Center · US

Funding

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
NCI NIH HHS P01 CA193124
6 · The paper itself

Abstract

Here, we survey the diverse functions of DNA polymerase ζ (pol ζ) in eukaryotes. In mammalian cells, REV3L (3130 residues) is the largest catalytic subunit of the DNA polymerases. The orthologous subunit in yeast is Rev3p. Pol ζ also includes REV7 subunits (encoded by Rev7 in yeast and MAD2L2 in mammalian cells) and two subunits shared with the replicative DNA polymerase, pol δ. Pol ζ is used in response to circumstances that stall DNA replication forks in both yeast and mammalian cells. The best-examined situation is translesion synthesis at sites of covalent DNA lesions such as UV radiation-induced photoproducts. We also highlight recent evidence that uncovers various roles of pol ζ that extend beyond translesion synthesis. For instance, pol ζ is also employed when the replisome operates sub-optimally or at difficult-to-replicate DNA sequences. Pol ζ also participates in repair by microhomology mediated break-induced replication. A rev3 deletion is tolerated in yeast but Rev3l disruption results in embryonic lethality in mice. Inactivation of mammalian Rev3l results in genomic instability and invokes cell death and senescence programs. Targeting of pol ζ function may be a useful strategy in cancer therapy, although chromosomal instability associated with pol ζ deficiency must be considered.

Indexed as

DNA RepairAnimalsCell DeathCellular SenescenceDNA-Binding ProteinsDNA DamageDNA-Directed DNA PolymeraseDNA ReplicationEmbryo, MammalianGenomic InstabilityHumansMiceSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsUltraviolet RaysDNA-Binding ProteinsDNA-Directed DNA PolymeraseREV3L protein, humanREV3L protein, mouseREV3 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID31410467
PMCPMC6895278
OpenAlexW2967431278

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.