Evidence map›Paper›PMID 32188865›Full record

ArticleScientific reports2020

RAB5A and TRAPPC6B are novel targets for Shiga toxin 2a inactivation in kidney epithelial cells.

Ivan U Kouzel, Alexander Kehl, Petya Berger, Ivan Liashkovich, Daniel Steil, Wojciech Makalowski, Yutaka Suzuki, Gottfried Pohlentz, Helge Karch, Alexander Mellmann and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. EnterohemorrhagicInternational journal of molecular sciences · 2022
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Molecular Biology ofToxins · 2020
    Review
  9. 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

11 authors at 2 institutions in 3 countries.

Ivan U Kouzel *Institute for Hygiene and National Consulting Laboratory for Hemolytic Uremic Syndrome (HUS), University of Münster, D-48149, Münster, Germany. Ivan.Kouzel@uib.no.ORCID http://orcid.org/0000-0001-9868-2174
Alexander Kehl *Institute for Hygiene and National Consulting Laboratory for Hemolytic Uremic Syndrome (HUS), University of Münster, D-48149, Münster, Germany. alexander.kehl@ukmuenster.de.ORCID http://orcid.org/0000-0002-1127-8847
Petya BergerInstitute for Hygiene and National Consulting Laboratory for Hemolytic Uremic Syndrome (HUS), University of Münster, D-48149, Münster, Germany.
Ivan LiashkovichInstitute for Physiology II, University of Münster, D-48149, Münster, Germany.
Daniel SteilInstitute for Hygiene and National Consulting Laboratory for Hemolytic Uremic Syndrome (HUS), University of Münster, D-48149, Münster, Germany.
Wojciech MakalowskiInstitute of Bioinformatics, University of Münster, D-48149, Münster, Germany.ORCID http://orcid.org/0000-0003-2303-9541
Yutaka SuzukiDepartment of Computational Biology and Medical Sciences, University of Tokyo, 277-8562, Tokyo, Japan.
Gottfried PohlentzInstitute for Hygiene and National Consulting Laboratory for Hemolytic Uremic Syndrome (HUS), University of Münster, D-48149, Münster, Germany.
Helge KarchInstitute for Hygiene and National Consulting Laboratory for Hemolytic Uremic Syndrome (HUS), University of Münster, D-48149, Münster, Germany.
Alexander MellmannInstitute for Hygiene and National Consulting Laboratory for Hemolytic Uremic Syndrome (HUS), University of Münster, D-48149, Münster, Germany.ORCID http://orcid.org/0000-0002-0649-5185
Johannes MüthingInstitute for Hygiene and National Consulting Laboratory for Hemolytic Uremic Syndrome (HUS), University of Münster, D-48149, Münster, Germany.
University of Münster · DEThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cardinal virulence factor of human-pathogenic enterohaemorrhagic Escherichia coli (EHEC) is Shiga toxin (Stx), which causes severe extraintestinal complications including kidney failure by damaging renal endothelial cells. In EHEC pathogenesis, the disturbance of the kidney epithelium by Stx becomes increasingly recognised, but how this exactly occurs is unknown. To explore this molecularly, we investigated the Stx receptor content and transcriptomic profile of two human renal epithelial cell lines: highly Stx-sensitive ACHN cells and largely Stx-insensitive Caki-2 cells. Though both lines exhibited the Stx receptor globotriaosylceramide, RNAseq revealed strikingly different transcriptomic responses to an Stx challenge. Using RNAi to silence factors involved in ACHN cells' Stx response, the greatest protection occurred when silencing RAB5A and TRAPPC6B, two host factors that we newly link to Stx trafficking. Silencing these factors alongside YKT6 fully prevented the cytotoxic Stx effect. Overall, our approach reveals novel subcellular targets for potential therapies against Stx-mediated kidney failure.

Indexed as

Cells, CulturedEpithelial CellsGene Expression ProfilingGene Expression RegulationHumansKidneyrab5 GTP-Binding ProteinsShiga Toxin 2Vesicular Transport ProteinsRAB5C protein, humanrab5 GTP-Binding ProteinsShiga Toxin 2TRAPPC6B protein, humanVesicular Transport Proteins

Identifiers

PMID32188865
PMCPMC7080763
OpenAlexW3012414258

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.