Evidence map›Paper›PMID 9234787›Full record

ArticleInfection and immunity1997

Activation of host cell protein kinase C by enteropathogenic Escherichia coli.

J K Crane, J S Oh

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 85 citations in OpenAlex.

  1. Observational
  2. EnterohemorrhagicFrontiers in cell and developmental biology · 2020
    Article
  3. Article
  4. Review
  5. Pathogen-induced secretory diarrhea and its prevention.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Enteropathogenic E. coli-induced barrier function alteration is not a consequence of host cell apoptosis.American journal of physiology. Gastrointestinal and liver physiology · 2008
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

2 authors at 1 institution in 1 country.

J K CraneDepartment of Medicine, State University of New York at Buffalo, 14214, USA. jcrane@acsu.buffalo.edu
J S Oh
University at Buffalo, State University of New York · US

Funding

CGMP-LINKED RECEPTORS FOR THE ENTEROTOXIN STA OF E COLIR29DK049410 · NIDDK · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI CRANE, JOHN K. · 1994 to 1998
–
NIDDK NIH HHS R29 DK 49410
6 · The paper itself

Abstract

Enteropathogenic Escherichia coli (EPEC) consists of a group of diarrhea-producing E. coli strains, common in developing countries, which do not produce classical toxins and are not truly invasive. EPEC strains adhere to mammalian cells in an intimate fashion, trigger a localized increase in intracellular calcium levels, and elevate inositol phosphate production. We hypothesized that these mediators could activate host cell protein kinase C (PKC) and tested this idea in vitro with two cultured human cell lines, HeLa cells and T84 cells. Using a recently described subculturing protocol to "induce" or accelerate EPEC adherence, we infected the cells with EPEC at a multiplicity of infection of approximately 100:1 for 30 to 60 min. Under these conditions, EPEC E2348 increased membrane-bound PKC activity 1.5- to 2.3-fold in HeLa cells and T84 cells, respectively. The increase in membrane-bound PKC activity was accompanied by a decrease in cytosolic PKC activity in EPEC-infected HeLa cells. Nonadherent laboratory E. coli strains such as HB101 and H.S. failed to trigger any consistent change in PKC production, similar to the nonadherent mutant strains derived from E2348, JPN15 (plasmid cured) and CVD206 (eaeA). In addition, immunoblots performed on extracts of T84 cells with a monoclonal antibody against PKC-alpha showed an increased PKC content in membranes of EPEC-infected cells. Finally, EPEC-infected T84 cells showed a 60% increase in responsiveness to the E. coli heat-stable toxin. We conclude that mediators produced in response to EPEC adherence activate PKC in intestinal and nonintestinal cells.

Indexed as

Bacterial ToxinsCyclic GMPDiarrheaEnterotoxinsEnzyme ActivationEscherichia coliEscherichia coli ProteinsHumansProtein Kinase CStaurosporineTetradecanoylphorbol AcetateTumor Cells, CulturedBacterial ToxinsCyclic GMPEnterotoxinsEscherichia coli Proteinsheat stable toxin (E coli)Protein Kinase CStaurosporineTetradecanoylphorbol Acetate

Identifiers

PMID9234787
PMCPMC175464
OpenAlexW2137494670

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.