A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1
By J. Hampe, Andre Franke, P. Rosenstiel, A. Till, M. Teuber, K. Huse, Mario Albrecht, G. Mayr, F. M. D. L. Vega, Jason C. Briggs and 11 more. Nature Genetics, 2007
1,956 citations recorded by the source corpus.
Subfields: Genetics, Hematology, Public Health, Environmental and Occupational Health
View Paper: https://www.semanticscholar.org/paper/06e92f2e9ddae43d3188051f87fce744ebe844ca
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In Genetics
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In Hematology
In Public Health, Environmental and Occupational Health
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Citations in the corpus
- Mechanisms of Disease: Inflammatory Bowel Diseases. (2019, background): “Not only through NOD2 but also via CD risk locus ATG16L1, Paneth cells function in autophagy is compromised in patients with CD (25, 75).”
- Trait-Associated SNPs Are More Likely to Be eQTLs: Annotation to Enhance Discovery from GWAS (2010, background): “For a few disorders, results of GWAS have highlighted biological contributing factors to disease that had not previously been recognized as central, such as the complement system in macular degeneration [1] or autophagy in Crohn’s disease [2–4].”
- Genome-wide association study identifies new susceptibility loci for Crohn disease and implicates autophagy in disease pathogenesis (2007, background): “This SNP, which causes a nonsynonymous amino acid change in exon 8 (A197T), was recently show”
- The genetics and immunopathogenesis of inflammatory bowel disease (2008, background): “In the ATG16L1 gene, a SNP (Ala281Thr) was found to be highly associated with Crohn's disease, with the less common threonine allele conferring protection from the diseas”
- Genetics and pathogenesis of inflammatory bowel disease (2011, background): “Autophagy and IBD Genetic analyses have shown an unsuspected role for autophagy in innate immunity and IBD, implicating two component genes, ATG16L1 and IRGM , in IBD pathogenesi”