Nod2 Mutation in Crohn's Disease Potentiates NF-κB Activity and IL-1ß Processing
By S. Maeda, L. Hsu, Hongjun Liu, L. Bankston, M. Iimura, M. Kagnoff, L. Eckmann, M. Karin. Science, 2005
735 citations recorded by the source corpus.
Subfields: Epidemiology, Genetics, Immunology
View Paper: https://www.semanticscholar.org/paper/2cffcaf802f356dbe005340dfd1db82f2e6c73a0
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Citations in the corpus
- Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer. (2006, background): “Inhibition of IL-1b signaling by injection of IL-1 receptor antagonist (IL-1Ra) inhibited DSS-induced colonic inflammation and abolished the phenotypic differences between the Nod2 knockin mice and wild-type counterparts (Maeda et al., 2005a).”
- Inflammation and cancer: An ancient link with novel potentials (2007, background): “These mutations enhance NF-jB activity and increased the production of IL-1b.(79) Although the majority of evidence supports a role of NF-jB in tumor progression, its antitumorigenic function has also been reported in certain cell types (reviewed in Ref.”
- TLR Signaling in the Gut in Health and Disease1 (2005, background): “E-mail address: Maria.Abreu@mssm.edu 3 Abbreviations used in this paper: NOD, nucleotide oligomerization domain; PAMP, pathogen-associated molecular pattern; IEC, intestinal epithelial cell; LTA, lipotechoic acid; IRAK, IL-1 receptor-associated kinase; IBD, inflammatory bowel disease; DSS, dextran s”
- The inflammasomes: guardians of the body. (2009, background): “NOD2 has also been suggested to play a role, together with NALP1, in MDP-induced caspase-1 activation, further suggesting that multiple NLRs may cooperate and synergize to mount host defenses (68, 165).”
- The gut flora as a forgotten organ (2006, background): “For example, TLR2 is activated by peptidoglycan and lipotechoic acids, TLR4 by lipopolysaccharide, TLR5 by flagellin, and NOD1/ CARD4 and NOD2/CARD15 function as intracellular receptors of peptidoglycan subunits.”