Evidence map›Paper›PMID 24587136›Full record

ArticlePloS one2014

The oxidative stress responsive transcription factor Pap1 confers DNA damage resistance on checkpoint-deficient fission yeast cells.

Carrie Belfield, Craig Queenan, Hui Rao, Kenji Kitamura, Nancy C Walworth

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Molecular biology research communications · 2018
    Article
  3. Article
  4. Article
  5. Review
  6. 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

5 authors at 4 institutions in 2 countries.

Carrie BelfieldDepartment of Pharmacology, Rutgers Robert Wood Johnson Medical School, Piscataway, New Jersey, United States of America ; Graduate Program in Cellular and Molecular Pharmacology, Rutgers Graduate School of Biomedical Sciences, Piscataway, New Jersey, United States of America.
Craig QueenanDepartment of Pharmacology, Rutgers Robert Wood Johnson Medical School, Piscataway, New Jersey, United States of America.
Hui RaoDepartment of Pharmacology, Rutgers Robert Wood Johnson Medical School, Piscataway, New Jersey, United States of America.
Kenji KitamuraCenter for Gene Science, Hiroshima University, Higashi-Hiroshima, Japan.
Nancy C WalworthDepartment of Pharmacology, Rutgers Robert Wood Johnson Medical School, Piscataway, New Jersey, United States of America ; Graduate Program in Cellular and Molecular Pharmacology, Rutgers Graduate School of Biomedical Sciences, Piscataway, New Jersey, United States of America ; Member, Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey, United States of America.
Rutgers, The State University of New Jersey · USHiroshima University · JPJohnson University · USRutgers Cancer Institute of New Jersey

Funding

UMDNJ-RUTGERS UNIVERSITY PIPELINE PROGRAMR25GM055145 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HAIMOVICH, BEATRICE, LANGER, JEROME ALAN · 1996 to 2020
$8.7M
Cell Cycle Checkpoint in Response to DNA DamageR01GM053194 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI WALWORTH, NANCY C. · 1995 to 2011
$4.4M
NIGMS NIH HHS R01 GM053194NIGMS NIH HHS R25 GM055145
6 · The paper itself

Abstract

Eukaryotic cells invoke mechanisms to promote survival when confronted with cellular stress or damage to the genome. The protein kinase Chk1 is an integral and conserved component of the DNA damage response pathway. Mutation or inhibition of Chk1 results in mitotic death when cells are exposed to DNA damage. Oxidative stress activates a pathway that results in nuclear accumulation of the bZIP transcription factor Pap1. We report the novel finding that fission yeast Pap1 confers resistance to drug- and non-drug-induced DNA damage even when the DNA damage checkpoint is compromised. Multi-copy expression of Pap1 restores growth to chk1-deficient cells exposed to camptothecin or hydroxyurea. Unexpectedly, increased Pap1 expression also promotes survival of chk1-deficient cells with mutations in genes encoding DNA ligase (cdc17) or DNA polymerase δ (cdc6), but not DNA replication initiation mutants. The ability of Pap1 to confer resistance to DNA damage was not specific to chk1 mutants, as it also improved survival of rad1- and rad9-deficient cells in the presence of CPT. To confer resistance to DNA damage Pap1 must localize to the nucleus and be transcriptionally active.

Indexed as

Basic-Leucine Zipper Transcription FactorsCamptothecinCell NucleusCheckpoint Kinase 1DNA DamageDNA LigasesHydroxyureaMicroscopy, FluorescenceOxidative StressPancreatitis-Associated ProteinsProtein KinasesSchizosaccharomycesSchizosaccharomyces pombe ProteinsBasic-Leucine Zipper Transcription FactorsCamptothecinCdc17 protein, S pombecdc6 protein, S pombeCheckpoint Kinase 1Chk1 protein, S pombeDNA LigasesHydroxyureaPancreatitis-Associated ProteinsPap1 protein, S pombeProtein KinasesREG3A protein, humanSchizosaccharomyces pombe Proteins

Identifiers

PMID24587136
PMCPMC3934961
OpenAlexW2060602976

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.