Evidence map›Paper›PMID 24643541›Full record

ArticleInfection and immunity2014

EspC promotes epithelial cell detachment by enteropathogenic Escherichia coli via sequential cleavages of a cytoskeletal protein and then focal adhesion proteins.

Fernando Navarro-Garcia, Antonio Serapio-Palacios, Jorge E Vidal, M Isabel Salazar, Gabriela Tapia-Pastrana

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  7. Sialic acid plays a pivotal role in licensingProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  8. Article
  9. Review
  10. Enteropathogenic Escherichia coli Infection in Cancer and Immunosuppressed Patients.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021
    Article
  11. Manipulation of Focal Adhesion Signaling by Pathogenic Microbes.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. The Role of Nonerythroid SpectrinJournal of oncology · 2019
    Review
  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

5 authors at 1 institution in 1 country.

Fernando Navarro-GarciaDepartment of Cell Biology, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Mexico City, Mexico.
Antonio Serapio-Palacios
Jorge E Vidal
M Isabel Salazar
Gabriela Tapia-Pastrana
Center for Research and Advanced Studies of the National Polytechnic Institute · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

EspC is a non-locus of enterocyte effacement (LEE)-encoded autotransporter produced by enteropathogenic Escherichia coli (EPEC) that is secreted to the extracellular milieu by a type V secretion system and then translocated into epithelial cells by the type III secretion system. Here, we show that this efficient EspC delivery into the cell leads to a cytopathic effect characterized by cell rounding and cell detachment. Thus, EspC is the main protein involved in epithelial cell cytotoxicity detected during EPEC adhesion and pedestal formation assays. The cell detachment phenotype is triggered by cytoskeletal and focal adhesion disruption. EspC-producing EPEC is able to cleave fodrin, paxillin, and focal adhesion kinase (FAK), but these effects are not observed when cells are infected with an espC isogenic mutant. Recovery of these phenotypes by complementing the mutant with the espC gene but not with the espC gene mutated in the serine protease motif highlights the role of the protease activity of EspC in the cell detachment phenotype. In vitro assays using purified proteins showed that EspC, but not EspC with an S256I substitution [EspCS256I], directly cleaves these cytoskeletal and focal adhesion proteins. Kinetics of protein degradation indicated that EspC-producing EPEC first cleaves fodrin (within the 11th and 9th repetitive units at the Q1219 and D938 residues, respectively), and this event sequentially triggers paxillin degradation, FAK dephosphorylation, and FAK degradation. Thus, cytoskeletal and focal adhesion protein cleavage leads to the cell rounding and cell detachment promoted by EspC-producing EPEC.

Indexed as

Bacterial AdhesionCarrier ProteinsCell AdhesionCell LineEnteropathogenic Escherichia coliEpithelial CellsEscherichia coli InfectionsEscherichia coli ProteinsFocal Adhesion Protein-Tyrosine KinasesHumansMicrofilament ProteinsPaxillinSpectrinCarrier ProteinsEscherichia coli ProteinsEspC protein, E coliFocal Adhesion Protein-Tyrosine KinasesMicrofilament ProteinsPaxillinSpectrin

Identifiers

PMID24643541
PMCPMC4019189
OpenAlexW2024558947

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.