Evidence map›Paper›PMID 16428723›Full record

ArticleInfection and immunity2006

Analysis of the function of enteropathogenic Escherichia coli EspB by random mutagenesis.

Wensheng Luo, Michael S Donnenberg

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Assay for Type III Secretion in Escherichia coli.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Enteropathogenic escherichia coli infection in children.Current opinion in infectious diseases · 2011
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Pathophysiology of EnteropathogenicNewborn (Clarksville, Md.)
    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.

Wensheng LuoDivision of Infectious Diseases, University of Maryland School of Medicine, 20 Penn St., Baltimore, MD 21201, USA.
Michael S Donnenberg
University of Maryland, Baltimore · US

Funding

The eae Gene Cluster of Enteropathogenic E.coliR01AI032074 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI DONNENBERG, MICHAEL S · 1997 to 2012
$3.7M
The eae Gene Cluster of Enteropathogenic E.coliR56AI032074 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI DONNENBERG, MICHAEL S · 2007 to 2007
$375k
EAE GENE CLUSTER OF ENTEROPATHOGENIC E. COLIR29AI032074 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI DONNENBERG, MICHAEL S · 1992 to 1996
–
NIAID NIH HHS AI32074NIAID NIH HHS R01 AI032074NIAID NIH HHS R56 AI032074
6 · The paper itself

Abstract

Enteropathogenic Escherichia coli (EPEC) is an important cause of infantile diarrhea, especially in developing countries. EspB, a key virulence factor of EPEC, is required for the attaching and effacing effect characteristic of EPEC and enterohemorrhagic E. coli and has been posited to play several functions in the process of infection. Attaching and effacing activity is associated with the accumulation of filamentous actin beneath adherent bacteria as measured in the fluorescence actin staining (FAS) test. To determine whether different domains of EspB are responsible for different functions, 42 plasmids carrying mutated espB were introduced into an espB deletion mutant. Two major groups of espB mutants were identified. One group of 17 mutants exhibited positive FAS results and normal levels of hemolytic activity. Another group of 22 mutants exhibited negative FAS results and low levels of hemolytic activity. Three mutants were exceptional. One mutant was FAS positive but had significantly reduced hemolytic activity. Conversely, a second mutant was FAS negative but had full hemolytic activity. A third mutant had a significantly reduced FAS level compared to the wild type but full hemolytic activity. The results of EspF and Tir translocation assays confirmed that FAS-negative insertions disrupt effector translocation and mutants with FAS-positive insertions retain protein translocation activity. These results suggest that EspB has distinct domain functions involved in effector translocation that can be distinguished from its role as a component of the translocation pore.

Indexed as

Gene DeletionMutagenesis, InsertionalActinsAmino Acid SequenceAnimalsBacterial AdhesionBacterial Outer Membrane ProteinsDiarrhea, InfantileEscherichia coliEscherichia coli ProteinsHeLa CellsHemolysisHumansInfant, NewbornMolecular Sequence DataPlasmidsActinsBacterial Outer Membrane ProteinsEaeB protein, E coliEscherichia coli ProteinsReceptors, Cell SurfaceTir protein, E coli

Identifiers

PMID16428723
PMCPMC1360311
OpenAlexW2139094950

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.