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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5710
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pubmed:dateCreated |
2005-2-4
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pubmed:abstractText |
Variants of NOD2, an intracellular sensor of bacteria-derived muramyl dipeptide (MDP), increase susceptibility to Crohn's disease (CD). These variants are thought to be defective in activation of nuclear factor kappaB (NF-kappaB) and antibacterial defenses, but CD clinical specimens display elevated NF-kappaB activity. To illuminate the pathophysiological function of NOD2, we introduced such a variant to the mouse Nod2 locus. Mutant mice exhibited elevated NF-kappaB activation in response to MDP and more efficient processing and secretion of the cytokine interleukin-1beta (IL-1beta). These effects are linked to increased susceptibility to bacterial-induced intestinal inflammation and identify NOD2 as a positive regulator of NF-kappaB activation and IL-1beta secretion.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetylmuramyl-Alanyl-Isoglutamine,
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Bacterial Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Card15 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Dextran Sulfate,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Nod2 Signaling Adaptor Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Peptidoglycan
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1095-9203
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
4
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pubmed:volume |
307
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
734-8
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pubmed:dateRevised |
2011-7-18
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pubmed:meshHeading |
pubmed-meshheading:15692052-Acetylmuramyl-Alanyl-Isoglutamine,
pubmed-meshheading:15692052-Animals,
pubmed-meshheading:15692052-Anti-Bacterial Agents,
pubmed-meshheading:15692052-Apoptosis,
pubmed-meshheading:15692052-Bacteria,
pubmed-meshheading:15692052-Cells, Cultured,
pubmed-meshheading:15692052-Colitis,
pubmed-meshheading:15692052-Colon,
pubmed-meshheading:15692052-Crohn Disease,
pubmed-meshheading:15692052-Cytokines,
pubmed-meshheading:15692052-Dextran Sulfate,
pubmed-meshheading:15692052-Interleukin-1,
pubmed-meshheading:15692052-Intestinal Mucosa,
pubmed-meshheading:15692052-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:15692052-Lipopolysaccharides,
pubmed-meshheading:15692052-Macrophage Activation,
pubmed-meshheading:15692052-Macrophages,
pubmed-meshheading:15692052-Mice,
pubmed-meshheading:15692052-Mutation,
pubmed-meshheading:15692052-NF-kappa B,
pubmed-meshheading:15692052-Nod2 Signaling Adaptor Protein,
pubmed-meshheading:15692052-Peptidoglycan,
pubmed-meshheading:15692052-Signal Transduction
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pubmed:year |
2005
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pubmed:articleTitle |
Nod2 mutation in Crohn's disease potentiates NF-kappaB activity and IL-1beta processing.
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pubmed:affiliation |
Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0723, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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