Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Contributions of IBD5, IL23R, ATG16L1, and NOD2 to Crohn's disease risk in a population-based case-control study: evidence of gene-gene interactions.

Inflammatory bowel diseases - 1 Nov 2008

Okazaki Toshihiko, Wang Ming-Hsi, Rawsthorne Patricia, Sargent Michael, Datta Lisa Wu, Shugart Yin Yao, Bernstein Charles N, Brant Steven R

Abstract excerpt

BACKGROUND: IBD5, IL23R, and ATG16L1 genetic variations are established Crohn's disease (CD) risks alleles. We evaluated these in a population-based case-control study within a cohort to determine their penetrance, population attributable risk, independence, and relationship to other established CD risk factors, including NOD2. METHODS: DNA from 213 CD, 118 [corrected] ulcerative colitis, and 315 [corrected]...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Colitis, Ulcerative
Share to Crohn Disease

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Incidence

Share to Logistic Models

Share to Nod2 Signaling Adaptor Protein

Share to Receptors, Interleukin

Share to Reference Values

Share to Registries

Source

Open in PubMed Open full text

Identifiers

PMID: 18521914
DOI: 10.1002/ibd.20512
PMCID: PMC3336049

Genes

NOD2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Contributions of IBD5, IL23R, ATG16L1, and NOD2 to Crohn's disease risk in a population-based case-control study: evidence of gene-gene interactions.PMID 18521914Read ↗

Genome-wide association study of Crohn's disease in Koreans revealed three new susceptibility loci and common attributes of genetic susceptibility across ethnic populations.Semantic proximity Read ↗

IL23R R381Q and ATG16L1 T300A are strongly associated with Crohn's disease in a study of New Zealand Caucasians with inflammatory bowel disease.Semantic proximity Read ↗

ATG16L1 and IL23R variants and genetic susceptibility to crohn's disease: mode of inheritance based on meta-analysis of genetic association studies.Semantic proximity Read ↗

The expanding universe of inflammatory bowel disease genetics.Semantic proximity Read ↗

Role of ATG16L, NOD2 and IL23R in Crohn's disease pathogenesis.Semantic proximity Read ↗

Update on genetics in inflammatory disease.Semantic proximity Read ↗

Genetics of inflammatory bowel disease: clues to pathogenesis.Semantic proximity Read ↗

Molecular prediction of disease risk and severity in a large Dutch Crohn's disease cohort.Semantic proximity Read ↗

The ATG16L1 gene variants rs2241879 and rs2241880 (T300A) are strongly associated with susceptibility to Crohn's disease in the German population.Semantic proximity Read ↗

Genetic determinants of ulcerative colitis include the ECM1 locus and five loci implicated in Crohn's disease.Semantic proximity Read ↗

Crohn's Disease Susceptibility Gene Interactions, a NOD to the Newcomer ATG16L1Semantic proximity Read ↗

The genetics and immunopathogenesis of inflammatory bowel disease.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.