Evidence map›Paper›PMID 17684544›Full record

ArticlePloS one2007

Systematic association mapping identifies NELL1 as a novel IBD disease gene.

Andre Franke, Jochen Hampe, Philip Rosenstiel, Christian Becker, Florian Wagner, Robert Häsler, Randall D Little, Klaus Huse, Andreas Ruether, Tobias Balschun and 15 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 3 pooled it
10.9field-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

55 citing papers in PubMed, 3 syntheses or guidelines pooled it, 138 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. NELL-1: role and mechanisms in disease pathogenesis and development.Frontiers in cell and developmental biology · 2026
    Review
  5. Article
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  9. Isolation of NELL 1 Aptamers for Rhabdomyosarcoma Targeting.Bioengineering (Basel, Switzerland) · 2022
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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

25 authors at 7 institutions in 2 countries.

Andre FrankeInstitute for Clinical Molecular Biology, Christian-Albrechts University Kiel, Kiel, Germany.
Jochen Hampe
Philip Rosenstiel
Christian Becker
Florian Wagner
Robert Häsler
Randall D Little
Klaus Huse
Andreas Ruether
Tobias Balschun
Michael Wittig
Abdou Elsharawy
Gabriele Mayr
Mario Albrecht
Natalie J Prescott
Clive M Onnie
Hélène Fournier
Tim Keith
Uwe Radelof
Matthias Platzer
Christopher G Mathew
Monika Stoll
Michael Krawczak
Peter Nürnberg
Stefan Schreiber
Christian-Albrechts-Universität zu Kiel · DEKing's College School · GBGerman Center for Infection Research · DELeibniz Association · DEMax Planck Institute for Informatics · DEUniversity of Cologne · DEUniversity of Lübeck · DE

Funding

Medical Research Council G0000934Wellcome Trust
6 · The paper itself

Abstract

Crohn disease (CD), a sub-entity of inflammatory bowel disease (IBD), is a complex polygenic disorder. Although recent studies have successfully identified CD-associated genetic variants, these susceptibility loci explain only a fraction of the heritability of the disease. Here, we report on a multi-stage genome-wide scan of 393 German CD cases and 399 controls. Among the 116,161 single-nucleotide polymorphisms tested, an association with the known CD susceptibility gene NOD2, the 5q31 haplotype, and the recently reported CD locus at 5p13.1 was confirmed. In addition, SNP rs1793004 in the gene encoding nel-like 1 precursor (NELL1, chromosome 11p15.1) showed a consistent disease-association in independent German population- and family-based samples (942 cases, 1082 controls, 375 trios). Subsequent fine mapping and replication in an independent sample of 454 French/Canadian CD trios supported the authenticity of the NELL1 association. Further confirmation in a large German ulcerative colitis (UC) sample indicated that NELL1 is a ubiquitous IBD susceptibility locus (combined p<10(-6); OR = 1.66, 95% CI: 1.30-2.11). The novel 5p13.1 locus was also replicated in the French/Canadian sample and in an independent UK CD patient panel (453 cases, 521 controls, combined p<10(-6) for SNP rs1992660). Several associations were replicated in at least one independent sample, point to an involvement of ITGB6 (upstream), GRM8 (downstream), OR5V1 (downstream), PPP3R2 (downstream), NM_152575 (upstream) and HNF4G (intron).

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyCalcium-Binding ProteinsChromosome MappingColitis, UlcerativeCrohn DiseaseGenotypeHaplotypesHumansInflammatory Bowel DiseasesModels, MolecularMolecular Sequence DataNerve Tissue ProteinsOligonucleotide Array Sequence AnalysisPolymorphism, Single NucleotideProtein Structure, TertiaryCalcium-Binding ProteinsNELL1 protein, humanNerve Tissue Proteins

Identifiers

PMID17684544
PMCPMC1933598
OpenAlexW2023454175

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.