Evidence map›Paper›PMID 9707589›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Generation of a strong mutator phenotype in yeast by imbalanced base excision repair.

B J Glassner, L J Rasmussen, M T Najarian, L M Posnick, L D Samson

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

80 citing papers in PubMed, 190 citations in OpenAlex.

  1. Article
  2. Article
  3. Decoding mitochondrial DNA damage and repair associated withFrontiers in cellular and infection microbiology · 2024
    Review
  4. International journal of molecular sciences · 2023
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  5. Article
  6. Article
  7. The complexity and regulation of repair of alkylation damage to nucleic acids.Critical reviews in biochemistry and molecular biology · 2021
    Review
  8. Article
  9. Article
  10. Tools and systems for evolutionary engineering of biomolecules and microorganisms.Journal of industrial microbiology & biotechnology · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

20 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

5 authors at 1 institution in 1 country.

B J GlassnerDepartment of Cancer Cell Biology, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA.
L J Rasmussen
M T Najarian
L M Posnick
L D Samson
Harvard University · US

Funding

RADIATION BIOLOGY TRAINING PROGRAMT32CA009078 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI D'ANDREA, ALAN D. · 1985 to 2009
$4.6M
STUDIES OF DNA REPAIR USING RHIZOBIUM MELILOTIP01ES003926 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WALKER, GRAHAM C · 1985 to 1997
–
NCI NIH HHS 5T32CA09078-19NCI NIH HHS R01-CA5502NCI NIH HHS T32 CA009078NIEHS NIH HHS P01-ES03926
6 · The paper itself

Abstract

Increased spontaneous mutation is associated with increased cancer risk. Here, by using a model system, we show that spontaneous mutation can be increased several hundred-fold by a simple imbalance between the first two enzymes involved in DNA base excision repair. The Saccharomyces cerevisiae MAG1 3-methyladenine (3MeA) DNA glycosylase, when expressed at high levels relative to the apurinic/apyrimidinic endonuclease, increases spontaneous mutation by up to approximately 600-fold in S. cerevisiae and approximately 200-fold in Escherichia coli. Genetic evidence suggests that, in yeast, the increased spontaneous mutation requires the generation of abasic sites and the processing of these sites by the REV1/REV3/REV7 lesion bypass pathway. Comparison of the mutator activity produced by Mag1, which has a broad substrate range, with that produced by the E. coli Tag 3MeA DNA glycosylase, which has a narrow substrate range, indicates that the removal of endogenously produced 3MeA is unlikely to be responsible for the mutator effect of Mag1. Finally, the human AAG 3-MeA DNA glycosylase also can produce a small (approximately 2-fold) but statistically significant increase in spontaneous mutation, a result which could have important implications for carcinogenesis.

Indexed as

DNA GlycosylasesEscherichia coli ProteinsMutationCarbon-Oxygen LyasesDeoxyribonuclease IV (Phage T4-Induced)DNA-(Apurinic or Apyrimidinic Site) LyaseDNA RepairEscherichia coliGene ExpressionGenes, FungalHumansMethyl MethanesulfonateMutagensNeoplasmsN-Glycosyl HydrolasesPhenotype3-methyladenine-DNA glycosylaseCarbon-Oxygen LyasesDeoxyribonuclease IV (Phage T4-Induced)DNA-(Apurinic or Apyrimidinic Site) LyaseDNA Glycosylasesendonuclease IV, E coliEscherichia coli ProteinsMethyl MethanesulfonateMutagensN-Glycosyl Hydrolases

Identifiers

PMID9707589
PMCPMC21450
OpenAlexW2092243514

What OpenQuestion holds

Textmetadata
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.