Evidence map›Paper›PMID 21926160›Full record

ArticleNucleic acids research2012

REV1 and polymerase ζ facilitate homologous recombination repair.

Shilpy Sharma, J Kevin Hicks, Colleen L Chute, Julia R Brennan, Joon-Young Ahn, Thomas W Glover, Christine E Canman

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
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  6. Review
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  8. Article
  9. Host translesion polymerases are required for viral genome integrity.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Article
  11. Article
  12. Article
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  15. Article
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  18. REV7: Jack of many trades.Trends in cell biology · 2021
    Review
  19. Review
  20. Article

18 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

7 authors at 1 institution in 1 country.

Shilpy SharmaDepartment of Pharmacology, The University of Michigan Medical School, Ann Arbor, Michigan 48109, USA.
J Kevin Hicks
Colleen L Chute
Julia R Brennan
Joon-Young Ahn
Thomas W Glover
Christine E Canman
University of Michigan–Ann Arbor · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Scott Michael Schuetze · 1988 to 2026
$178.2M
INTERDEPARTMENTAL TRAINING IN PHARMACOLOGICAL SCIENCEST32GM007767 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ISOM, LORI L. · 1985 to 2019
$10.2M
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 5 P30 CA46592NCI NIH HHS CA133046NCI NIH HHS R01 CA133046NIGMS NIH HHS GM007767
6 · The paper itself

Abstract

REV1 and DNA Polymerase ζ (REV3 and REV7) play important roles in translesion DNA synthesis (TLS) in which DNA replication bypasses blocking lesions. REV1 and Polζ have also been implicated in promoting repair of DNA double-stranded breaks (DSBs). However, the mechanism by which these two TLS polymerases increase tolerance to DSBs is poorly understood. Here we demonstrate that full-length human REV1, REV3 and REV7 interact in vivo (as determined by co-immunoprecipitation studies) and together, promote homologous recombination repair. Cells lacking REV3 were hypersensitive to agents that cause DSBs including the PARP inhibitor, olaparib. REV1, REV3 or REV7-depleted cells displayed increased chromosomal aberrations, residual DSBs and sites of HR repair following exposure to ionizing radiation. Notably, cells depleted of DNA polymerase η (Polη) or the E3 ubiquitin ligase RAD18 were proficient in DSB repair following exposure to IR indicating that Polη-dependent lesion bypass or RAD18-dependent monoubiquitination of PCNA are not necessary to promote REV1 and Polζ-dependent DNA repair. Thus, the REV1/Polζ complex maintains genomic stability by directly participating in DSB repair in addition to the canonical TLS pathway.

Indexed as

Recombinational DNA RepairCells, CulturedChromosomal InstabilityDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA-Directed DNA PolymeraseHumansMad2 ProteinsNuclear ProteinsNucleotidyltransferasesProteinsRadiation, IonizingRadiation ToleranceY-Family DNA PolymerasesDNA-Binding ProteinsDNA-Directed DNA PolymeraseMAD2L2 protein, humanMad2 ProteinsNuclear ProteinsNucleotidyltransferasesProteinsREV1 protein, humanREV3L protein, humanY-Family DNA Polymerases

Identifiers

PMID21926160
PMCPMC3258153
OpenAlexW2053851495

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.