Evidence map›Paper›PMID 21564333›Full record

ArticleMolecular microbiology2011

Nitrosative damage to free and zinc-bound cysteine thiols underlies nitric oxide toxicity in wild-type Borrelia burgdorferi.

Travis J Bourret, Julie A Boylan, Kevin A Lawrence, Frank C Gherardini

Open access · hybridAbstract read
In one paragraph

Article in Molecular microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 52 citations in OpenAlex.

  1. Comparative evaluation of viability assays and functional analysis ofApplied and environmental microbiology · 2026
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  4. Frontiers in immunology · 2026
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  8. A putative xanthine dehydrogenase is critical forMicrobiology (Reading, England) · 2023
    Article
  9. Review
  10. Complex Interplay of Heme-Copper Oxidases with Nitrite and Nitric Oxide.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Lyme Disease Pathogenesis.Current issues in molecular biology · 2021
    Review
  15. Article
  16. Interactions between Borrelia burgdorferi and ticks.Nature reviews. Microbiology · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Travis J BourretLaboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4th Street, Hamilton, MT 59840, USA.
Julie A Boylan
Kevin A Lawrence
Frank C Gherardini
National Institutes of Health · US

Funding

The Roles of Key Transcription Factors on the Pathogenesis of B. Burgdorferi, the Causative Agent of Lyme DiseaseZIAAI000905 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI GHERARDINI, FRANK · 2009 to 2023
$12.4M
Intramural NIH HHS
6 · The paper itself

Abstract

Borrelia burgdorferi encounters potentially harmful reactive nitrogen species (RNS) throughout its infective cycle. In this study, diethylamine NONOate (DEA/NO) was used to characterize the lethal effects of RNS on B. burgdorferi. RNS produce a variety of DNA lesions in a broad spectrum of microbial pathogens; however, levels of the DNA deamination product, deoxyinosine, and the numbers of apurinic/apyrimidinic (AP) sites were identical in DNA isolated from untreated and DEA/NO-treated B. burgdorferi cells. Strains with mutations in the nucleotide excision repair (NER) pathway genes uvrC or uvrB treated with DEA/NO had significantly higher spontaneous mutation frequencies, increased numbers of AP sites in DNA and reduced survival compared with wild-type controls. Polyunsaturated fatty acids in B. burgdorferi cell membranes, which are susceptible to peroxidation by reactive oxygen species (ROS), were not sensitive to RNS-mediated lipid peroxidation. However, treatment of B. burgdorferi cells with DEA/NO resulted in nitrosative damage to several proteins, including the zinc-dependent glycolytic enzyme fructose-1,6-bisphosphate aldolase (BB0445), the Borrelia oxidative stress regulator (BosR) and neutrophil-activating protein (NapA). Collectively, these data suggested that nitrosative damage to proteins harbouring free or zinc-bound cysteine thiols, rather than DNA or membrane lipids underlies RNS toxicity in wild-type B. burgdorferi.

Indexed as

Bacterial ProteinsBorrelia burgdorferiChemokines, CXCCysteineFructose-Bisphosphate AldolaseNitric OxideNitrosationSulfhydryl CompoundsTrans-ActivatorsZincBacterial ProteinsChemokines, CXCCysteinecysteine thiolateFructose-Bisphosphate AldolaseNapA protein, Borrelia burgdorferiNitric OxideSulfhydryl CompoundsTrans-ActivatorsZinc

Identifiers

PMID21564333
PMCPMC3147059
OpenAlexW2096258348

What OpenQuestion holds

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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.