Evidence map›Paper›PMID 21245842›Full record

ArticleNature communications2011

PAR2 absence completely rescues inflammation and ichthyosis caused by altered CAP1/Prss8 expression in mouse skin.

Simona Frateschi, Eric Camerer, Giovanna Crisante, Sarah Rieser, Mathieu Membrez, Roch-Philippe Charles, Friedrich Beermann, Jean-Christophe Stehle, Bernadette Breiden, Konrad Sandhoff and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.0field-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

58 citing papers in PubMed, 113 citations in OpenAlex.

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  17. ENaC activation by proteases.Acta physiologica (Oxford, England) · 2022
    Review
  18. Article
  19. Article
  20. Trypsin-Like Proteases and Their Role in Muco-Obstructive Lung Diseases.International journal of molecular sciences · 2021
    Review
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

17 authors at 7 institutions in 4 countries.

Simona FrateschiDepartment of Pharmacology and Toxicology, University of Lausanne, Lausanne 1005, Switzerland.
Eric Camerer
Giovanna Crisante
Sarah Rieser
Mathieu Membrez
Roch-Philippe Charles
Friedrich Beermann
Jean-Christophe Stehle
Bernadette Breiden
Konrad Sandhoff
Samuel Rotman
Marek Haftek
Anne Wilson
Stephan Ryser
Martin Steinhoff
Shaun R Coughlin
Edith Hummler
University of Lausanne · CHUniversity of California, San Francisco · USUniversity of Bonn · DEÉcole Polytechnique Fédérale de Lausanne · CHFondation de l'Avenir · FRLudwig Cancer Research · CHUniversité Claude Bernard Lyon 1 · FR

Funding

Cytokine Signaling in Neurons: Inflammation, Pain and PruritisR01AR059402 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STEINHOFF, MARTIN · 2011 to 2013
$1.0M
NIAMS NIH HHS R01 AR059402
6 · The paper itself

Abstract

Altered serine protease activity is associated with skin disorders in humans and in mice. The serine protease channel-activating protease-1 (CAP1; also termed protease serine S1 family member 8 (Prss8)) is important for epidermal homeostasis and is thus indispensable for postnatal survival in mice, but its roles and effectors in skin pathology are poorly defined. In this paper, we report that transgenic expression in mouse skin of either CAP1/Prss8 (K14-CAP1/Prss8) or protease-activated receptor-2 (PAR2; Grhl3(PAR2/+)), one candidate downstream target, causes epidermal hyperplasia, ichthyosis and itching. K14-CAP1/Prss8 ectopic expression impairs epidermal barrier function and causes skin inflammation characterized by an increase in thymic stromal lymphopoietin levels and immune cell infiltrations. Strikingly, both gross and functional K14-CAP1/Prss8-induced phenotypes are completely negated when superimposed on a PAR2-null background, establishing PAR2 as a pivotal mediator of pathogenesis. Our data provide genetic evidence for PAR2 as a downstream effector of CAP1/Prss8 in a signalling cascade that may provide novel therapeutic targets for ichthyoses, pruritus and inflammatory skin diseases.

Identifiers

PMID21245842
PMCPMC3105307
OpenAlexW1989100246

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.