Evidence map›Paper›PMID 28620161›Full record

ArticleScientific reports2017

Different signaling patterns contribute to loss of keratinocyte cohesion dependent on autoantibody profile in pemphigus.

Elias Walter, Franziska Vielmuth, Lukas Rotkopf, Miklós Sárdy, Orsolya N Horváth, Matthias Goebeler, Enno Schmidt, Rüdiger Eming, Michael Hertl, Volker Spindler and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
4.8field-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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

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  7. Dsg3 epitope-specific signalling in pemphigus.Frontiers in immunology · 2023
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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

11 authors at 4 institutions in 1 country.

Elias WalterInstitute of Anatomy and Cell Biology, Ludwig-Maximilians-Universität München, Munich, 80336, Germany.
Franziska VielmuthInstitute of Anatomy and Cell Biology, Ludwig-Maximilians-Universität München, Munich, 80336, Germany.
Lukas RotkopfInstitute of Anatomy and Cell Biology, Ludwig-Maximilians-Universität München, Munich, 80336, Germany.ORCID 0000-0001-9862-218X
Miklós SárdyDepartment of Dermatology and Allergology, Ludwig-Maximilians-Universität München, Munich, 80336, Germany.
Orsolya N HorváthDepartment of Dermatology and Allergology, Ludwig-Maximilians-Universität München, Munich, 80336, Germany.
Matthias GoebelerDepartment of Dermatology, Venerology and Allergology, University Hospital Würzburg, Würzburg, 97080, Germany.
Enno SchmidtLübeck Institute of Experimental Dermatology (Lied), University of Lübeck, Lübeck, 23562, Germany.
Rüdiger EmingDepartment of Dermatology and Allergology, Philipps-Universität Marburg, Marburg, 35037, Germany.
Michael HertlDepartment of Dermatology and Allergology, Philipps-Universität Marburg, Marburg, 35037, Germany.
Volker SpindlerInstitute of Anatomy and Cell Biology, Ludwig-Maximilians-Universität München, Munich, 80336, Germany. Volker.Spindler@med.uni-muenchen.de.
Jens WaschkeInstitute of Anatomy and Cell Biology, Ludwig-Maximilians-Universität München, Munich, 80336, Germany. Jens.Waschke@med.uni-muenchen.de.
Ludwig-Maximilians-Universität München · DEPhilipps University of Marburg · DEUniversitätsklinikum Würzburg · DEUniversity of Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pemphigus is an autoimmune blistering skin disease caused primarily by autoantibodies against desmoglein (Dsg)1 and 3. Here, we characterized the mechanisms engaged by pemphigus IgG from patients with different clinical phenotypes and autoantibody profiles. All pemphigus vulgaris (PV) and pemphigus foliaceus (PF) IgG and AK23, a monoclonal mouse antibody against Dsg3, caused loss of cell cohesion, cytokeratin retraction and p38MAPK activation. Strong alterations in Dsg3 distribution were caused by mucosal (aDsg3 antibodies), mucocutaneous (aDsg1 + aDsg3) as well as atypical (aDsg3) PV-IgG. All PV-IgG fractions and AK23 compromised Dsg3 but not Dsg1 binding and enhanced Src activity. In contrast, rapid Ca

Indexed as

Cell AdhesionSignal TransductionAnimalsAntibodies, MonoclonalAutoantibodiesDesmoglein 1Desmoglein 3HumansImmunoglobulin GKeratinocytesKeratinsMicePemphigusAntibodies, MonoclonalAutoantibodiesDesmoglein 1Desmoglein 3DSG1 protein, humanDSG3 protein, humanImmunoglobulin GKeratins

Identifiers

PMID28620161
PMCPMC5472593
OpenAlexW2621473839

What OpenQuestion holds

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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.