Evidence map›Paper›PMID 19216740›Full record

ArticleBMC systems biology2009

A module-based analytical strategy to identify novel disease-associated genes shows an inhibitory role for interleukin 7 Receptor in allergic inflammation.

Reza Mobini, Bengt A Andersson, Jonas Erjefält, Mirjana Hahn-Zoric, Michael A Langston, Andy D Perkins, Lars Olaf Cardell, Mikael Benson

Open access · diamondAbstract read
In one paragraph

Article in BMC systems biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

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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

8 authors at 4 institutions in 2 countries.

Reza MobiniUnit for Clinical Systems Biology, Department of Pediatrics, University of Gothenburg, Gothenburg, Sweden. reza.mobini@pediat.gu.se
Bengt A Andersson
Jonas Erjefält
Mirjana Hahn-Zoric
Michael A Langston
Andy D Perkins
Lars Olaf Cardell
Mikael Benson
University of Gothenburg · SEUniversity of Tennessee at Knoxville · USKarolinska Institutet · SELund University · SE

Funding

Bioinfomatics for Mouse Phenotype AnalysisP01DA015027 · NIDA · UNIVERSITY OF TENNESSEE KNOXVILLE · PI LANGSTON, MICHAEL ALLEN · 2002 to 2004
$1.8M
INIA: Informatics CoreU01AA013512 · NIAAA · UNIVERSITY OF TENNESSEE KNOXVILLE · PI LANGSTON, MICHAEL ALLEN · 2002 to 2006
$1.5M
NIAAA NIH HHS 5-U01-AA-013512-02NIAAA NIH HHS U01 AA013512NIDA NIH HHS 1-P01-DA-015027-01NIDA NIH HHS P01 DA015027NIMH NIH HHS 1-R01-MH-074460-01
6 · The paper itself

Abstract

backgroundThe identification of novel genes by high-throughput studies of complex diseases is complicated by the large number of potential genes. However, since disease-associated genes tend to interact, one solution is to arrange them in modules based on co-expression data and known gene interactions. The hypothesis of this study was that such a module could be a) found and validated in allergic disease and b) used to find and validate one ore more novel disease-associated genes.

resultsTo test these hypotheses integrated analysis of a large number of gene expression microarray experiments from different forms of allergy was performed. This led to the identification of an experimentally validated reference gene that was used to construct a module of co-expressed and interacting genes. This module was validated in an independent material, by replicating the expression changes in allergen-challenged CD4+ cells. Moreover, the changes were reversed following treatment with corticosteroids. The module contained several novel disease-associated genes, of which the one with the highest number of interactions with known disease genes, IL7R, was selected for further validation. The expression levels of IL7R in allergen challenged CD4+ cells decreased following challenge but increased after treatment. This suggested an inhibitory role, which was confirmed by functional studies.

conclusionWe propose that a module-based analytical strategy is generally applicable to find novel genes in complex diseases.

Indexed as

Adrenal Cortex HormonesCD4-Positive T-LymphocytesGATA3 Transcription FactorGene Expression ProfilingGene Expression RegulationHumansHypersensitivityOligonucleotide Array Sequence AnalysisReceptors, Interleukin-7Statistics, NonparametricAdrenal Cortex HormonesGATA3 protein, humanGATA3 Transcription FactorReceptors, Interleukin-7

Identifiers

PMID19216740
PMCPMC2653464
OpenAlexW2053266278

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LicenceCC BY
Read underepoch 390

Registered trials

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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.