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No association between the functional CARD4 insertion/deletion polymorphism and inflammatory bowel diseases in the German population

¹ Institute for Clinical Molecular Biology, Christian-Albrechts-University, Kiel, Germany
² Medical Department, Rikshospitalet University Hospital, Oslo, Norway
³ Institute for Clinical Molecular Biology, Christian-Albrechts-University, Kiel, Germany

Correspondence to:
Correspondence to:
Dr S Schreiber
Institute for Clinical Molecular Biology, Christian-Albrechts-University, Schittenhelmstrasse 12, 24105 Kiel, Germany; s.schreiber@mucosa.de

Keywords: CARD4; NOD1; Germany; inflammatory bowel disease; caspase recruitment domain family; member 15; Crohn’s disease; nucleotide binding oligomerisation domain protein 2; ulcerative colitis

The first 150 words of the full text of this article appear below.

Inflammatory bowel diseases (IBD, OMIM 601458 [OMIM] ) are represented by two main subtypes, Crohn’s disease (CD, OMIM 266600 [OMIM] ) and ulcerative colitis (UC, OMIM 191390 [OMIM] ). The first and most widely replicated susceptibility gene for CD is CARD15 (caspase recruitment domain family, member 15) that encodes NOD2 (nucleotide binding oligomerisation domain protein 2), a protein involved in the pathogen associated molecular pattern recognition system (for review see Schreiber and colleagues¹). Identification of functional CARD15 variants revealed the important role of impaired barrier integrity and host defence in the pathogenesis of CD and other inflammatory diseases.¹ Recently, an association between IBD and variants in the CARD4 gene, which encodes NOD1, a structural homologue of NOD2, has been demonstrated in the British population.² In that study, McGovern et al identified the common (deletion) allele of the marker ND₁+32656 as a risk factor for IBD. Conversely, the minor ND₁+32656 allele, . . . [Full text of this article]

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