Evidence map›Paper›PMID 33303781›Full record

ArticleScientific reports2020

Cathepsin S provokes interleukin-6 (IL-6) trans-signaling through cleavage of the IL-6 receptor in vitro.

Charlotte M Flynn, Yvonne Garbers, Stefan Düsterhöft, Rielana Wichert, Juliane Lokau, Christian H K Lehmann, Diana Dudziak, Bernd Schröder, Christoph Becker-Pauly, Stefan Rose-John and 2 more

Open access · goldAbstract read
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 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. Genome-wide studies define new genetic mechanisms of IgA vasculitis.medRxiv : the preprint server for health sciences · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Article
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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

12 authors at 5 institutions in 1 country.

Charlotte M FlynnInstitute of Biochemistry, Kiel University, Kiel, Germany.
Yvonne GarbersInstitute of Psychology, Kiel University, Kiel, Germany.
Stefan DüsterhöftInstitute of Molecular Pharmacology, RWTH Aachen University, Aachen, Germany.
Rielana WichertInstitute of Biochemistry, Kiel University, Kiel, Germany.
Juliane LokauDepartment of Pathology, Medical Faculty, Otto-Von-Guericke-University Magdeburg, Magdeburg, Germany.
Christian H K LehmannLaboratory of Dendritic Cell Biology, Department of Dermatology, University Hospital Erlangen, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany.
Diana DudziakLaboratory of Dendritic Cell Biology, Department of Dermatology, University Hospital Erlangen, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany.
Bernd SchröderInstitute for Physiological Chemistry, Medizinisch-Theoretisches Zentrum MTZ, Technische Universität Dresden, Fiedlerstraße 42, 01307, Dresden, Germany.
Christoph Becker-PaulyInstitute of Biochemistry, Kiel University, Kiel, Germany.
Stefan Rose-JohnInstitute of Biochemistry, Kiel University, Kiel, Germany.
Samadhi Aparicio-SiegmundInstitute of Biochemistry, Kiel University, Kiel, Germany.
Christoph GarbersDepartment of Pathology, Medical Faculty, Otto-Von-Guericke-University Magdeburg, Magdeburg, Germany. christoph.garbers@med.ovgu.de.
Kiel University · DEOtto-von-Guericke University Magdeburg · DEUniversitätsklinikum Erlangen · DERWTH Aachen University · DETU Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cytokine interleukin-6 (IL-6) fulfills its pleiotropic functions via different modes of signaling. Regenerative and anti-inflammatory activities are mediated via classic signaling, in which IL-6 binds to the membrane-bound IL-6 receptor (IL-6R). For IL-6 trans-signaling, which accounts for the pro-inflammatory properties of the cytokine, IL-6 activates its target cells via soluble forms of the IL-6R (sIL-6R). We have previously shown that the majority of sIL-6R in human serum originates from proteolytic cleavage and mapped the cleavage site of the IL-6R. The cleavage occurs between Pro-355 and Val-356, which is the same cleavage site that the metalloprotease ADAM17 uses in vitro. However, sIL-6R serum levels are unchanged in hypomorphic ADAM17

Indexed as

AnimalsCathepsinsHumansHydrolysisInterleukin-6In Vitro TechniquesMiceReceptors, Interleukin-6Signal Transductioncathepsin SCathepsinsIL6 protein, humanInterleukin-6Receptors, Interleukin-6

Identifiers

PMID33303781
PMCPMC7730449
OpenAlexW3112345432

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.