Evidence map›Paper›PMID 23195997›Full record

ReviewMutation research

The roles of DNA polymerase ζ and the Y family DNA polymerases in promoting or preventing genome instability.

Shilpy Sharma, Corey M Helchowski, Christine E Canman

Abstract readReview
In one paragraph

Review in Mutation research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
–field-weighted citation impact
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

42 citing papers in PubMed.

  1. Review
  2. Mad2B forms a complex with Cdc20, Cdc27, Rev3 and Rev1 in response to cisplatin-induced DNA damage.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
    Article
  3. Article
  4. Article
  5. Article
  6. Protein-Protein Interactions in Translesion Synthesis.Molecules (Basel, Switzerland) · 2021
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. DNA polymerase δ proofreads errors made by DNA polymerase ε.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Article
  13. DNA-Histone Cross-Links: Formation and Repair.Frontiers in cell and developmental biology · 2020
    Review
  14. Article
  15. Article
  16. Review
  17. Translesion DNA polymerases in eukaryotes: what makes them tick?Critical reviews in biochemistry and molecular biology · 2017
    Review
  18. Review
  19. Review
  20. Review
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

3 authors.

Shilpy SharmaDepartment of Pharmacology, University of Michigan, Ann Arbor, MI 48109, United States.
Corey M HelchowskiDepartment of Pharmacology, University of Michigan, Ann Arbor, MI 48109, United States.
Christine E CanmanDepartment of Pharmacology, University of Michigan, Ann Arbor, MI 48109, United States. Electronic address: ccanman@umich.edu.

Funding

Training Program in Tumor MicroenvironmentT32CA009676 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Maria G Castro, Analisa Virginia DiFeo · 1992 to 2026
$7.3M
Novel mechanisms by which REV1 and POLZ affect response to anticancer agentsR01CA133046 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CANMAN, CHRISTINE ELIZABETH · 2008 to 2018
$3.0M
NCI NIH HHS CA133046NCI NIH HHS R01 CA133046NCI NIH HHS T32 CA009676NCI NIH HHS T32CA009676-20
6 · The paper itself

Abstract

Cancer cells display numerous abnormal characteristics which are initiated and maintained by elevated mutation rates and genome instability. Chromosomal DNA is continuously surveyed for the presence of damage or blocked replication forks by the DNA Damage Response (DDR) network. The DDR is complex and includes activation of cell cycle checkpoints, DNA repair, gene transcription, and induction of apoptosis. Duplicating a damaged genome is associated with elevated risks to fork collapse and genome instability. Therefore, the DNA damage tolerance (DDT) pathway is also employed to enhance survival and involves the recruitment of translesion DNA synthesis (TLS) polymerases to sites of replication fork blockade or single stranded DNA gaps left after the completion of replication in order to restore DNA to its double stranded form before mitosis. TLS polymerases are specialized for inserting nucleotides opposite DNA adducts, abasic sites, or DNA crosslinks. By definition, the DDT pathway is not involved in the actual repair of damaged DNA, but provides a mechanism to tolerate DNA lesions during replication thereby increasing survival and lessening the chance for genome instability. However this may be associated with increased mutagenesis. In this review, we will describe the specialized functions of Y family polymerases (Rev1, Polη, Polι and Polκ) and DNA polymerase ζ in lesion bypass, mutagenesis, and prevention of genome instability, the latter due to newly appreciated roles in DNA repair. The recently described role of the Fanconi anemia pathway in regulating Rev1 and Polζ-dependent TLS is also discussed in terms of their involvement in TLS, interstrand crosslink repair, and homologous recombination.

Indexed as

DNA DamageDNA RepairGenomic InstabilityAnimalsDNA-Directed DNA PolymeraseDNA ReplicationHumansDNA-Directed DNA PolymeraseDNA polymerase zeta

Identifiers

PMID23195997
PMCPMC3616148

What OpenQuestion holds

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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.