Evidence map›Paper›PMID 24397487›Full record

ArticleMolecular microbiology2014

EmrA1 membrane fusion protein of Francisella tularensis LVS is required for resistance to oxidative stress, intramacrophage survival and virulence in mice.

Zhuo Ma, Sukalyani Banik, Harshita Rane, Vanessa T Mora, Seham M Rabadi, Christopher R Doyle, David G Thanassi, Chandra Shekhar Bakshi, Meenakshi Malik

Open access · bronzeAbstract read
In one paragraph

Article in Molecular microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-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

24 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. TolC and EmrA1 contribute toJournal of bacteriology · 2024
    Article
  4. Article
  5. Implication of the σMicrobiology spectrum · 2023
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Genetic Determinants of Antibiotic Resistance inFrontiers in microbiology · 2021
    Review
  12. Contributions of TolC Orthologs toInfection and immunity · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. 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

9 authors at 3 institutions in 1 country.

Zhuo MaDepartment of Basic and Social Sciences, Albany College of Pharmacy and Health Sciences, Albany, New York, USA.
Sukalyani Banik
Harshita Rane
Vanessa T Mora
Seham M Rabadi
Christopher R Doyle
David G Thanassi
Chandra Shekhar Bakshi
Meenakshi Malik
New York Medical College · USAlbany College of Pharmacy and Health Sciences · USStony Brook University · US

Funding

TLR2/NLR Signal Regulation of Protective Immunity to F. TularensisP01AI056320 · NIAID · ALBANY MEDICAL COLLEGE · PI METZGER, DENNIS W · 2003 to 2016
$22.9M
Repression of Inflammasome by Francisella tularensisR15AI107698 · NIAID · ALBANY COLLEGE OF PHARMACY · PI MALIK, MEENAKSHI · 2013 to 2024
$1.9M
Modulation of macrophage function by Francisella tularensisR56AI090072 · NIAID · NEW YORK MEDICAL COLLEGE · PI BAKSHI, CHANDRA SHEKHAR · 2010 to 2010
$316k
NIAID NIH HHS 2P01AI056320NIAID NIH HHS P01 AI056320NIAID NIH HHS R15 AI107698NIAID NIH HHS R15AI107698NIAID NIH HHS R56 AI090072
6 · The paper itself

Abstract

Francisella tularensis is a category A biodefence agent that causes a fatal human disease known as tularaemia. The pathogenicity of F. tularensis depends on its ability to persist inside host immune cells primarily by resisting an attack from host-generated reactive oxygen and nitrogen species (ROS/RNS). Based on the ability of F. tularensis to resist high ROS/RNS levels, we have hypothesized that additional unknown factors act in conjunction with known antioxidant defences to render ROS resistance. By screening a transposon insertion library of F. tularensis LVS in the presence of hydrogen peroxide, we have identified an oxidant-sensitive mutant in putative EmrA1 (FTL_0687) secretion protein. The results demonstrate that the emrA1 mutant is highly sensitive to oxidants and several antimicrobial agents, and exhibits diminished intramacrophage growth that can be restored to wild-type F. tularensis LVS levels by either transcomplementation, inhibition of ROS generation or infection in NADPH oxidase deficient (gp91Phox(-/-)) macrophages. The emrA1 mutant is attenuated for virulence, which is restored by infection in gp91Phox(-/-) mice. Further, EmrA1 contributes to oxidative stress resistance by affecting secretion of Francisella antioxidant enzymes SodB and KatG. This study exposes unique links between transporter activity and the antioxidant defence mechanisms of F. tularensis.

Indexed as

Membrane FusionMicrobial ViabilityOxidative StressAmino Acid SequenceAnimalsAnti-Bacterial AgentsAntioxidantsBacterial ProteinsBacterial Secretion SystemsDrug Resistance, BacterialFrancisella tularensisGenome, BacterialHumansHydrogen PeroxideMacrophagesMembrane GlycoproteinsAnti-Bacterial AgentsAntioxidantsBacterial ProteinsBacterial Secretion SystemsCybb protein, mouseHydrogen PeroxideMembrane GlycoproteinsNADPH Oxidase 2NADPH Oxidases

Identifiers

PMID24397487
PMCPMC4097035
OpenAlexW1909453738

What OpenQuestion holds

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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.