Evidence map›Paper›PMID 19042977›Full record

ReviewNucleic acids research2009

Bacterial topoisomerase I as a target for discovery of antibacterial compounds.

Yuk-Ching Tse-Dinh

Open access · goldAbstract readReview
In one paragraph

Review in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

64 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
  2. Article
  3. Structural Mechanisms of Topoisomerase-Targeting Drugs.Annual review of biochemistry · 2025
    Review
  4. AApplied and environmental microbiology · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Bulge oligonucleotide as an inhibitory agent of bacterial topoisomerase I.Journal of enzyme inhibition and medicinal chemistry · 2018
    Article
  20. Article

4 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

1 author at 1 institution in 1 country.

Yuk-Ching Tse-DinhDepartment of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA. yuk-ching_tse-dinh@nymc.edu
New York Medical College · US

Funding

Supplement for undergraduate research participant to promote diversityR01GM054226 · NIGMS · NEW YORK MEDICAL COLLEGE · PI TSE-DINH, YUK-CHING · 1996 to 2020
$4.6M
Bacterial cell killing topoisomerase I--DNA lesionR01AI069313 · NIAID · NEW YORK MEDICAL COLLEGE · PI TSE-DINH, YUK-CHING · 2006 to 2014
$3.4M
NIAID NIH HHS R01 AI069313NIAID NIH HHS R01-AI6933NIGMS NIH HHS R01 GM054226NIGMS NIH HHS R01-GM54226
6 · The paper itself

Abstract

Bacterial topoisomerase I is a potential target for discovery of new antibacterial compounds. Mutant topoisomerases identified by SOS induction screening demonstrated that accumulation of the DNA cleavage complex formed by type IA topoisomerases is bactericidal. Characterization of these mutants of Yersinia pestis and Escherichia coli topoisomerase I showed that DNA religation can be inhibited while maintaining DNA cleavage activity by decreasing the binding affinity of Mg(II) ions. This can be accomplished either by mutation of the TOPRIM motif involved directly in Mg(II) binding or by altering the charge distribution of the active site region. Besides being used to elucidate the key elements for the control of the cleavage-religation equilibrium, the SOS-inducing mutants of Y. pestis and E. coli topoisomerase I have also been utilized as models to study the cellular response following the accumulation of bacterial topoisomerase I cleavage complex. Bacterial topoisomerase I is required for preventing hypernegative supercoiling of DNA during transcription. It plays an important role in transcription of stress genes during bacterial stress response. Topoisomerase I targeting poisons may be particularly effective when the bacterial pathogen is responding to host defense, or in the presence of other antibiotics that induce the bacterial stress response.

Indexed as

Topoisomerase I InhibitorsAnti-Bacterial AgentsBacteriaCell DeathDNA Topoisomerases, Type IDrug DiscoveryEnzyme InhibitorsMutationStress, PhysiologicalAnti-Bacterial AgentsDNA Topoisomerases, Type IEnzyme InhibitorsTopoisomerase I Inhibitors

Identifiers

PMID19042977
PMCPMC2647297
OpenAlexW2054166013

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.