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No association between the functional CARD4 insertion/deletion polymorphism and inflammatory bowel diseases in the German population
  1. A Franke1,
  2. A Ruether1,
  3. N Wedemeyer1,
  4. T H Karlsen2,
  5. A Nebel3,
  6. S Schreiber3
  1. 1Institute for Clinical Molecular Biology, Christian-Albrechts-University, Kiel, Germany
  2. 2Medical Department, Rikshospitalet University Hospital, Oslo, Norway
  3. 3Institute for Clinical Molecular Biology, Christian-Albrechts-University, Kiel, Germany
  1. Correspondence to:
    Dr S Schreiber
    Institute for Clinical Molecular Biology, Christian-Albrechts-University, Schittenhelmstrasse 12, 24105 Kiel, Germany; s.schreiber{at}mucosa.de

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Inflammatory bowel diseases (IBD, OMIM 601458) are represented by two main subtypes, Crohn’s disease (CD, OMIM 266600) and ulcerative colitis (UC, OMIM 191390). 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 …

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