Evidence map›Paper›PMID 27274359›Full record

ArticleGut pathogens2016

Calcium binding protects E-cadherin from cleavage by Helicobacter pylori HtrA.

Thomas P Schmidt, Camilla Goetz, Markus Huemer, Gisbert Schneider, Silja Wessler

Open access · goldAbstract read
In one paragraph

Article in Gut pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Distinct Modulation ofBiomolecules · 2026
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  5. Design of aFrontiers in immunology · 2024
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  6. The immunopathogenesis ofFrontiers in microbiology · 2024
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  11. Cells · 2020
    Review
  12. Article
  13. Extracellular Pneumococcal Serine Proteases Affect Nasopharyngeal Colonization.Frontiers in cellular and infection microbiology · 2020
    Article
  14. Article
  15. The unique trimeric assembly of the virulence factor HtrA fromThe Journal of biological chemistry · 2019
    Article
  16. Review
  17. Genetic populations and virulence factors of Helicobacter pylori.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2018
    Review
  18. Amino-Terminal Processing ofFrontiers in microbiology · 2018
    Article
  19. Review
  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 2 institutions in 2 countries.

Thomas P SchmidtCancer Cluster Salzburg, Department of Molecular Biology, Division of Microbiology, Paris-Lodron University, Salzburg, Austria.
Camilla GoetzCancer Cluster Salzburg, Department of Molecular Biology, Division of Microbiology, Paris-Lodron University, Salzburg, Austria.
Markus HuemerCancer Cluster Salzburg, Department of Molecular Biology, Division of Microbiology, Paris-Lodron University, Salzburg, Austria.
Gisbert SchneiderDepartment of Chemistry and Applied Biosciences, Swiss Federal Institute of Technology (ETH), Zurich, Switzerland.
Silja WesslerCancer Cluster Salzburg, Department of Molecular Biology, Division of Microbiology, Paris-Lodron University, Salzburg, Austria.
University of Salzburg · ATETH Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe cell adhesion and tumor suppressor protein E-cadherin is an important factor in the establishment and maintenance of epithelial integrity. E-cadherin is a single transmembrane protein, which consists of an intracellular domain (IC), a transmembrane domain (TD), and five extracellular domains (EC). EC domains form homophilic interactions in cis and trans that require calcium binding to the linker region between the EC domains. In our previous studies, we identified the serine protease high temperature requirement A (HtrA) from the human pathogen and class-I carcinogen Helicobacter pylori (H. pylori) as a bacterial E-cadherin-cleaving protease that targets the linker region of the EC domains, thereby disrupting gastric epithelial integrity. However, it remains unclear how calcium binding to the E-cadherin linker regions affects HtrA-mediated cleavage.

resultsInvestigating the influence of calcium on the HtrA-mediated cleavage of recombinant E-cadherin (rCdh1) in vitro, we tested different concentrations of calcium ions and the calcium chelator ethylenediaminetetraacetic acid (EDTA). Calcium efficiently reduced HtrA-mediated E-cadherin fragmentation. Conversely, the addition of EDTA strongly increased cleavage, resulting in a ladder of defined E-cadherin fragments. However, calcium ions did not affect HtrA oligomerization and protease activity as monitored by degradation of the universal protease substrate casein. Finally, addition of ethyleneglycol-bis-tetraacetic acid (EGTA) slightly enhanced E-cadherin cleavage during H. pylori infection of gastric epithelial cells.

conclusionsOur results suggest that calcium blocks HtrA-mediated cleavage by interfering with the accessibility of calcium-binding regions between the individual EC domains, which have been identified as cleavage sites of HtrA.

Indexed as

CalciumE-cadherinHelicobacter pyloriHtrAProtease

Identifiers

PMID27274359
PMCPMC4895972
OpenAlexW2417707556

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.