Evidence map›Paper›PMID 17620356›Full record

ArticleInfection and immunity2007

Influence of the Cpx extracytoplasmic-stress-responsive pathway on Yersinia sp.-eukaryotic cell contact.

Katrin E Carlsson, Junfa Liu, Petra J Edqvist, Matthew S Francis

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Anti-infective compounds forSustainable microbiology · 2026
    Review
  3. Article
  4. Review
  5. Cpx-signalling innpj antimicrobials and resistance · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Successful Host Adaptation of IncK2 Plasmids.Frontiers in microbiology · 2019
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Environmental Regulation of Yersinia Pathophysiology.Frontiers in cellular and infection microbiology · 2016
    Review
  15. Article
  16. Article
  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 2 countries.

Katrin E CarlssonDepartment of Molecular Biology, Umeå University, SE-901 87 Umeå, Sweden.
Junfa Liu
Petra J Edqvist
Matthew S Francis
Umeå University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The extracytoplasmic-stress-responsive CpxRA two-component signal transduction pathway allows bacteria to adapt to growth in extreme environments. It controls the production of periplasmic protein folding and degradation factors, which aids in the biogenesis of multicomponent virulence determinants that span the bacterial envelope. This is true of the Yersinia pseudotuberculosis Ysc-Yop type III secretion system. However, despite using a second-site suppressor mutation to restore Yop effector secretion by yersiniae defective in the CpxA sensor kinase, these bacteria poorly translocated Yops into target eukaryotic cells. Investigation of this phenotype herein revealed that the expression of genes which encode several surface-located adhesins is also influenced by the Cpx pathway. In particular, the expression and surface localization of invasin, an adhesin that engages beta1-integrins on the eukaryotic cell surface, are severely restricted by the removal of CpxA. This reduces bacterial association with eukaryotic cells, which could be suppressed by the ectopic production of CpxA, invasin, or RovA, a positive activator of inv expression. In turn, these infected eukaryotic cells then became susceptible to intoxication by translocated Yop effectors. In contrast, bacteria harboring an in-frame deletion of cpxR, which encodes the cognate response regulator, displayed an enhanced ability to interact with cell monolayers, as well as elevated inv and rovA transcription. This phenotype could be drastically suppressed by providing a wild-type copy of cpxR in trans. We propose a mechanism of inv regulation influenced by the direct negative effects of phosphorylated CpxR on inv and rovA transcription. In this fashion, sensing of extracytoplasmic stress by CpxAR contributes to productive Yersinia sp.-eukaryotic cell interactions.

Indexed as

Adhesins, BacterialBacterial ProteinsCytoplasmGene Expression Regulation, BacterialHeLa CellsHumansOxidative StressProtein KinasesSignal TransductionYersinia pseudotuberculosisAdhesins, BacterialBacterial ProteinsCpxA protein, bacteriaCpxR protein, Bacteriainvasin, YersiniaProtein Kinases

Identifiers

PMID17620356
PMCPMC1951158
OpenAlexW2167825293

What OpenQuestion holds

Textmetadata
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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.