Evidence map›Paper›PMID 19926649›Full record

ArticleMicrobiology (Reading, England)2010

Different effects of transcriptional regulators MarA, SoxS and Rob on susceptibility of Escherichia coli to cationic antimicrobial peptides (CAMPs): Rob-dependent CAMP induction of the marRAB operon.

Douglas M Warner, Stuart B Levy

Abstract read
In one paragraph

Article in Microbiology (Reading, England), 2010. 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
2.8field-weighted citation impact, top 11% 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, 56 citations in OpenAlex.

  1. Review
  2. Review
  3. Colistin Resistance in Bacteria: Current Updates on Mechanism of Action and Combating Strategies.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Colistin: Lights and Shadows of an Older Antibiotic.Molecules (Basel, Switzerland) · 2024
    Review
  8. Review
  9. Article
  10. Modulation ofBiomedicines · 2023
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  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

2 authors at 1 institution in 1 country.

Douglas M WarnerDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA 02111, USA.
Stuart B LevyDepartment of Medicine, Tufts University School of Medicine, Boston, MA 02111, USA.
Tufts University · US

Funding

The multiple antibiotic resistance (MAR)regulonR01AI056021 · NIAID · TUFTS UNIVERSITY BOSTON · PI LEVY, STUART B. · 2003 to 2017
$8.9M
PATHOBIOLOGY OF DIGESTIVE DISEASEST32DK007542 · NIDDK · TUFTS UNIVERSITY BOSTON · PI LISCUM, LAURA · 1986 to 2010
$3.5M
NIAID NIH HHS AI56021NIAID NIH HHS R01 AI056021NIDDK NIH HHS T32 DK007542NIDDK NIH HHS T32 DK07542
6 · The paper itself

Abstract

Cationic antimicrobial peptides (CAMPs), a component of the mammalian immune system, protect the host from bacterial infections. The roles of the Escherichia coli transcriptional regulators MarA, SoxS and Rob in susceptibility to these peptides were examined. Overexpression of marA, either in an antibiotic-resistant marR mutant or from a plasmid, decreased bacterial susceptibility to CAMPs. Overexpression of the soxS gene from a plasmid, which decreased susceptibility to antibiotics, unexpectedly caused no decrease in CAMP susceptibility; instead it produced increased susceptibility to different CAMPs. Deletion or overexpression of rob had little effect on CAMP susceptibility. The marRAB operon was upregulated when E. coli was incubated in sublethal amounts of CAMPs polymyxin B, LL-37 or human beta-defensin-1; however, this upregulation required Rob. Deletion of acrAB increased bacterial susceptibility to polymyxin B, LL-37 and human beta-defensin-1 peptides. Deletion of tolC yielded an even greater increase in susceptibility to these peptides and also led to increased susceptibility to human alpha-defensin-2. Inhibition of cellular proton-motive force increased peptide susceptibility for wild-type and acrAB deletion strains; however, it decreased susceptibility of tolC mutants. These findings demonstrate that CAMPs are both inducers of marA-mediated drug resistance through interaction with Rob and also substrates for efflux in E. coli. The three related transcriptional regulators show different effects on bacterial cell susceptibility to CAMPs.

Indexed as

OperonAmino Acid SequenceAntimicrobial Cationic PeptidesBacterial Outer Membrane ProteinsBacterial ProteinsCathelicidinsDNA-Binding ProteinsDrug Resistance, Multiple, BacterialEscherichia coliEscherichia coli ProteinsGenes, BacterialHumansMembrane Transport ProteinsPolymyxin BRepressor ProteinsTrans-ActivatorsAntimicrobial Cationic PeptidesBacterial Outer Membrane ProteinsBacterial ProteinsCathelicidinsDNA-Binding ProteinsEscherichia coli ProteinsMarA protein, E coliMarR protein, E coliMembrane Transport Proteinsmultiple antibiotic resistance protein BPolymyxin BRepressor ProteinsRob protein, E coliSoxS protein, E colitolC protein, E coliTrans-Activators

Identifiers

PMID19926649
PMCPMC2890090
OpenAlexW2149556251

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.