NOD2 (CARD15) mutations in Crohn’s disease are associated with diminished mucosal α-defensin expression
By J. Wehkamp, J. Harder, M. Weichenthal, M. Schwab, E. Schäffeler, M. Schlee, K. Herrlinger, A. Stallmach, F. Noack, P. Fritz and 4 more. Gut, 2004
680 citations recorded by the source corpus.
Subfields: Genetics, Immunology, Microbiology
View Paper: https://www.semanticscholar.org/paper/987278393eb740b0a12caf914193994ed417e46c
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Genetics
In Immunology
Citations in the corpus
- Mechanisms of probiotic actions - A review. (2010, background): “The induction of adefensins in Paneth cells is carried out by activation of the cytoplasmic receptor NOD2, which recognizes muramyl dipeptide (Wehkamp et al., 2004).”
- Innate and adaptive immunity in inflammatory bowel disease. (2014, background): “Interestingly, the reduced expression of HD5 and HD6 is even more pronounced in patients carrying the NOD2 frameshift susceptibility variant, suggesting that an antimicrobial peptide defect may represent at least one of the mechanisms responsible for NOD2-associated risk [17].”
- Function of Nod‐like receptors in microbial recognition and host defense (2009, background): “Notably, Nod2-deficient mice and CD patients harboring mutant Nod2 have reduced expression of a-defensins, a class of anti-microbial peptides produced by Paneth cells (25, 111, 113).”