Evidence map›Paper›PMID 22296581›Full record

ArticleMolecular microbiology2012

A network of enzymes involved in repair of oxidative DNA damage in Neisseria meningitidis.

Krzysztofa Nagorska, Jan Silhan, Yanwen Li, Vladimir Pelicic, Paul S Freemont, Geoff S Baldwin, Christoph M Tang

Open access · greenAbstract read
In one paragraph

Article in Molecular microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. The Host-Pathogen Interactions and Epicellular Lifestyle ofFrontiers in cellular and infection microbiology · 2022
    Review
  2. Inhibitors of DNA Glycosylases as Prospective Drugs.International journal of molecular sciences · 2020
    Review
  3. Article
  4. Article
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  7. Review
  8. Article
  9. Article
  10. Structural basis for the recognition and cleavage of abasic DNA in Neisseria meningitidis.Proceedings of the National Academy of Sciences of the United States of America · 2012
    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

7 authors at 3 institutions in 2 countries.

Krzysztofa Nagorska *Centre for Molecular Microbiology and Infection, Imperial College London, London, SW7 2AZ, UK.
Jan Silhan *Division of Molecular Biosciences, Imperial College London, London, SW7 2AZ, UK.
Yanwen LiCentre for Molecular Microbiology and Infection, Imperial College London, London, SW7 2AZ, UK.
Vladimir PelicicCentre for Molecular Microbiology and Infection, Imperial College London, London, SW7 2AZ, UK.
Paul S FreemontDivision of Molecular Biosciences, Imperial College London, London, SW7 2AZ, UK.
Geoff S BaldwinDivision of Molecular Biosciences, Imperial College London, London, SW7 2AZ, UK.
Christoph M TangCentre for Molecular Microbiology and Infection, Imperial College London, London, SW7 2AZ, UK.
Imperial College London · GBSouthern African Centre for Infectious Disease Surveillance · TZUniversity of Oxford · GB

Funding

Medical Research Council G0900888Wellcome Trust 084369
6 · The paper itself

Abstract

Although oxidative stress is a key aspect of innate immunity, little is known about how host-restricted pathogens successfully repair DNA damage. Base excision repair is responsible for correcting nucleobases damaged by oxidative stress, and is essential for bloodstream infection caused by the human pathogen, Neisseria meningitidis. We have characterized meningococcal base excision repair enzymes involved in the recognition and removal of damaged nucleobases, and incision of the DNA backbone. We demonstrate that the bi-functional glycosylase/lyases Nth and MutM share several overlapping activities and functional redundancy. However, MutM and other members of the GO system, which deal with 8-oxoG, a common lesion of oxidative damage, are not required for survival of N. meningitidis under oxidative stress. Instead, the mismatch repair pathway provides back-up for the GO system, while the lyase activity of Nth can substitute for the meningococcal AP endonuclease, NApe. Our genetic and biochemical evidence shows that DNA repair is achieved through a robust network of enzymes that provides a flexible system of DNA repair. This network is likely to reflect successful adaptation to the human nasopharynx, and might provide a paradigm for DNA repair in other prokaryotes.

Indexed as

DNA DamageDNA RepairOxidative StressBacterial ProteinsDeoxyribonuclease (Pyrimidine Dimer)DNA, BacterialDNA-Formamidopyrimidine GlycosylaseNeisseria meningitidisBacterial ProteinsDeoxyribonuclease (Pyrimidine Dimer)DNA, BacterialDNA-Formamidopyrimidine Glycosylase

Identifiers

PMID22296581
PMCPMC3749813
OpenAlexW1863886608

What OpenQuestion holds

Textmetadata
LicenceTDM
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.