Evidence map›Paper›PMID 20953186›Full record

ArticleNature genetics2010

Common variants at TRAF3IP2 are associated with susceptibility to psoriatic arthritis and psoriasis.

Ulrike Hüffmeier, Steffen Uebe, Arif B Ekici, John Bowes, Emiliano Giardina, Eleanor Korendowych, Kristina Juneblad, Maria Apel, Ross McManus, Pauline Ho and 20 more

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers, 13 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed, 13 pooled it
13.5field-weighted citation impact, top 1% 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

185 citing papers in PubMed, 13 syntheses or guidelines pooled it, 365 citations in OpenAlex.

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  8. Association of IL23R polymorphisms with psoriasis and psoriatic arthritis: a meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012
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125 more citing papers are in PubMed but not listed here.

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

30 authors at 16 institutions in 5 countries.

Ulrike HüffmeierInstitute of Human Genetics, University of Erlangen-Nuremberg, Erlangen, Germany.
Steffen Uebe
Arif B Ekici
John Bowes
Emiliano Giardina
Eleanor Korendowych
Kristina Juneblad
Maria Apel
Ross McManus
Pauline Ho
Ian N Bruce
Anthony W Ryan
Frank Behrens
Jesús Lascorz
Beate Böhm
Heiko Traupe
Jörg Lohmann
Christian Gieger
Heinz-Erich Wichmann
Christine Herold
Michael Steffens
Lars Klareskog
Thomas F Wienker
Oliver Fitzgerald
Gerd-Marie Alenius
Neil J McHugh
Giuseppe Novelli
Harald Burkhardt
Anne Barton
André Reis
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEGoethe University Frankfurt · DEManchester Academic Health Science Centre · GBHelmholtz Zentrum München · DEInstitut für Medizinische Biometrie, Informatik und Epidemiologie · DETrinity College Dublin · IEUmeå University · SEKarolinska Institutet · SEPoliclinico Tor Vergata · ITRoyal National Hospital for Rheumatic Diseases · GBUniversity College Dublin · IEUniversity of Bath · GBUniversity of Bonn · DEUniversity of Manchester · GBUniversity of Münster · DEUniversity of Rome Tor Vergata · IT

Funding

Arthritis Research UK 17552Wellcome TrustWellcome Trust 076113
6 · The paper itself

Abstract

Psoriatic arthritis (PsA) is an inflammatory joint disease that is distinct from other chronic arthritides and which is frequently accompanied by psoriasis vulgaris (PsV) and seronegativity for rheumatoid factor. We conducted a genome-wide association study in 609 German individuals with PsA (cases) and 990 controls with replication in 6 European cohorts including a total of 5,488 individuals. We replicated PsA associations at HLA-C and IL12B and identified a new association at TRAF3IP2 (rs13190932, P = 8.56 × 10⁻¹⁷). TRAF3IP2 was also associated with PsV in a German cohort including 2,040 individuals (rs13190932, P = 1.95 × 10⁻³). Sequencing of the exons of TRAF3IP2 identified a coding variant (p.Asp10Asn, rs33980500) as the most significantly associated SNP (P = 1.13 × 10⁻²⁰, odds ratio = 1.95). Functional assays showed reduced binding of this TRAF3IP2 variant to TRAF6, suggesting altered modulation of immunoregulatory signals through altered TRAF interactions as a new and shared pathway for PsA and PsV.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdaptor Proteins, Signal TransducingArthritis, PsoriaticChromosomes, Human, Pair 6Diseases in TwinsDNA ReplicationGenotypeHumansInterleukinsPsoriasisTumor Necrosis Factor Receptor-Associated Peptides and ProteinsTwins, MonozygoticAdaptor Proteins, Signal TransducingInterleukinsTRAF3IP2 protein, humanTumor Necrosis Factor Receptor-Associated Peptides and Proteins

Identifiers

PMID20953186
PMCPMC2981079
OpenAlexW2033342396

What OpenQuestion holds

Textmetadata
LicenceTDM
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.