EditorialGenome-Wide Association Studies Herald a New Era of Rapid Discoveries in Inflammatory Bowel Disease Research
References (34)
- et al.
Crohn’s disease-associated NOD2 variants share a signaling defect in response to lipopolysaccharide and peptidoglycan
Gastroenterology
(2003) - et al.
Nod2 is a general sensor of peptidoglycan through muramyl dipeptide (MDP) detection
J Biol Chem
(2003) - et al.
Host recognition of bacterial muramyl dipeptide mediated through NOD2Implications for Crohn’s disease
J Biol Chem
(2003) - et al.
Muramyl dipeptide and toll-like receptor sensitivity in NOD2-associated Crohn’s disease
Lancet
(2005) - et al.
The contribution of OCTN1/2 variants within the IBD5 locus to disease susceptibility and severity in Crohn’s disease
Gastroenterology
(2005) - et al.
IL23R variation determines susceptibility but not disease phenotype in inflammatory bowel disease
Gastroenterology
(2007) - et al.
The IL-23/Th(17) axis: therapeutic targets for autoimmune inflammation
Curr Opin Immunol
(2006) - et al.
A large-scale genetic association study confirms IL12B and leads to the identification of IL23R as psoriasis-risk genes
Am J Hum Genet
(2007) - et al.
A nonsynonymous SNP in ATG16L1 predisposes to ileal Crohn’s disease and is independent of CARD15 and IBD5
Gastroenterology
(2007) Autophagy in innate and adaptive immunity
Trends Immunol
(2005)
Inflammatory bowel disease
N Engl J Med
(2002)
Genetics of inflammatory bowel disease
Inflamm Bowel Dis
(1996)
HLA-DR and -DQ phenotypes in inflammatory bowel disease: a meta- analysis
Gut
(1999)
Inflammatory bowel disease susceptibility loci defined by genome scan meta-analysis of 1952 affected relative pairs
Hum Mol Genet
(2004)
Current status of genetics research in inflammatory bowel disease
Genes Immun
(2005)
Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn’s disease
Nature
(2001)
A frameshift mutation in NOD2 associated with susceptibility to Crohn’s disease
Nature
(2001)
Cited by (0)
Copyright © 2007 AGA Institute. Published by Elsevier Inc. All rights reserved.