Evidence map›Paper›PMID 18720471›Full record

ArticleInflammatory bowel diseases2009

MAGI2 genetic variation and inflammatory bowel disease.

Dermot P B McGovern, Kent D Taylor, Carol Landers, Carrie Derkowski, Deb Dutridge, Marla Dubinsky, Andy Ippoliti, Eric Vasiliauskas, Ling Mei, Emebet Mengesha and 4 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Inflammatory bowel diseases, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 52 citations in OpenAlex.

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  18. Interleukin 23 in Crohn's disease.Inflammatory bowel diseases · 2014
    Review
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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

14 authors at 1 institution in 1 country.

Dermot P B McGovernMedical Genetics Institute & Inflammatory Bowel Disease Center, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA. mcgovernd@cshs.org
Kent D Taylor
Carol Landers
Carrie Derkowski
Deb Dutridge
Marla Dubinsky
Andy Ippoliti
Eric Vasiliauskas
Ling Mei
Emebet Mengesha
Lily King
Sheila Pressman
Stephan R Targan
Jerome I Rotter
Cedars-Sinai Medical Center · US

Funding

Using polygenic scores to enhance both variant discovery, and understanding of functional consequences of genetic variation in IBD.P01DK046763 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI TARGAN, STEPHAN R. · 1992 to 2020
$31.1M
NIDDK NIH HHS P01 DK046763
6 · The paper itself

Abstract

backgroundDespite recent advances the majority of inflammatory bowel disease (IBD) susceptibility 'genes' remain undiscovered. Recent data suggest that autoimmune conditions may 'share' susceptibility loci. Epidemiological evidence indicates an association between celiac disease and IBD and both conditions demonstrate increased gut permeability. MAGI2, recently implicated in ulcerative colitis (UC) and celiac disease, encodes a scaffolding protein involved in epithelial integrity. Our aim was to test MAGI2 variants for association with IBD and also their role in determining intermediate hereditary phenotypes defined by antibody production to microbial antigens.

methodsWe genotyped 113 MAGI2 single nucleotide polymorphisms (SNPs) in 681 cases of Crohn's disease (CD), 259 UC cases, and 195 controls.

resultsThe most significant IBD association was in intron 6 (rs2160322, P = 0.009) and both UC (P = 0.006) and CD (P = 0.03) contributed to this association. The most significant CD association was with an intron 2 haplotype (rs7785088/rs323149/rs13246026, P = 0.002). We observed highly significant associations with UC in intron 6 (rs7803276/rs7803705, P = 0.002) and also significant associations in introns 2, 6, and 20. Significant associations were seen with: immunoglobulin G (IgG) anti-Saccharomyces cerevisiae antibodies (ASCA)-positive CD in intron 3 (P = 0.003), intron 6 (P = 0.003), and intron 20 (P = 0.001); anti-CBir1-positive CD in intron 3 (P = 0.0001) and intron 6 (P = 0.008); and anti-outer membrane porin C (OmpC)-positive CD in intron 3 (P = 0.0009), and intron 9 (P = 0.007). Quantitative antibody levels were also associated with variants in intron 4 (anti-IgA ASCA, P = 0.0003 and anti-IgG ASCA, P = 0.0002).

conclusionsThese findings support the significance of the epithelial barrier in IBD pathogenesis.

Indexed as

Adaptor Proteins, Signal TransducingAntibodies, BacterialAntibodies, FungalBiomarkersCarrier ProteinsCase-Control StudiesColitis, UlcerativeCrohn DiseaseGuanylate KinasesHaplotypesHumansImmunoglobulin AImmunoglobulin GPolymorphism, Single NucleotidePorinsProteinsAdaptor Proteins, Signal TransducingAntibodies, BacterialAntibodies, FungalBiomarkersCarrier ProteinsGuanylate KinasesImmunoglobulin AImmunoglobulin GMAGI2 protein, humanPorinsProteins

Identifiers

PMID18720471
PMCPMC2614310
OpenAlexW1996144078

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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.