Evidence map›Paper›PMID 28279077›Full record

ReviewCritical reviews in biochemistry and molecular biology2017

Translesion DNA polymerases in eukaryotes: what makes them tick?

Alexandra Vaisman, Roger Woodgate

Open access · bronzeAbstract readReview
In one paragraph

Review in Critical reviews in biochemistry and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed
13.8field-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

146 citing papers in PubMed, 250 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Sensitization of cancer cells to DNA-damaging agents by expression of the REV1 C-terminal domain: Implications for chemotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. eLife · 2024
    Article
  18. Article
  19. Review
  20. MAD2L2 Dimerization Is Not Essential for Mitotic Regulation.International journal of molecular sciences · 2024
    Article

86 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.

Alexandra Vaismana Laboratory of Genomic Integrity , National Institute of Child Health and Human Development, National Institutes of Health , Bethesda , MD , USA.
Roger Woodgatea Laboratory of Genomic Integrity , National Institute of Child Health and Human Development, National Institutes of Health , Bethesda , MD , USA.
National Institutes of Health · US

Funding

DNA Replication, Repair, and Mutagenesis In Eukaryotic And Prokaryotic CellsZIAHD001500 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI WOODGATE, ROGER · 2009 to 2025
$37.5M
DNA REPLICATION, REPAIR, AND MUTAGENESIS IN EUKARYOTIC AND PROKARYOTIC CELLSZ01HD001500 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI WOODGATE, ROGER · 1985 to 2008
$3.1M
Intramural NIH HHS Z01 HD001500
6 · The paper itself

Abstract

Life as we know it, simply would not exist without DNA replication. All living organisms utilize a complex machinery to duplicate their genomes and the central role in this machinery belongs to replicative DNA polymerases, enzymes that are specifically designed to copy DNA. "Hassle-free" DNA duplication exists only in an ideal world, while in real life, it is constantly threatened by a myriad of diverse challenges. Among the most pressing obstacles that replicative polymerases often cannot overcome by themselves are lesions that distort the structure of DNA. Despite elaborate systems that cells utilize to cleanse their genomes of damaged DNA, repair is often incomplete. The persistence of DNA lesions obstructing the cellular replicases can have deleterious consequences. One of the mechanisms allowing cells to complete replication is "Translesion DNA Synthesis (TLS)". TLS is intrinsically error-prone, but apparently, the potential downside of increased mutagenesis is a healthier outcome for the cell than incomplete replication. Although most of the currently identified eukaryotic DNA polymerases have been implicated in TLS, the best characterized are those belonging to the "Y-family" of DNA polymerases (pols η, ι, κ and Rev1), which are thought to play major roles in the TLS of persisting DNA lesions in coordination with the B-family polymerase, pol ζ. In this review, we summarize the unique features of these DNA polymerases by mainly focusing on their biochemical and structural characteristics, as well as potential protein-protein interactions with other critical factors affecting TLS regulation.

Indexed as

DNA DamageAnimalsDNA-Directed DNA PolymeraseDNA RepairDNA ReplicationHumansDNA-Directed DNA PolymeraseDNA polymerase familiesmutagenesisPCNAprotein interaction networkreplicative bypassTranslesion synthesisubiquitin

Identifiers

PMID28279077
PMCPMC5573590
OpenAlexW2594378117

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.