<i>Nod2</i> Mutation in Crohn's Disease Potentiates NF-κB Activity and IL-1ß Processing
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- Shin Maeda
- 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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- Li-Chung Hsu
- 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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- Hongjun Liu
- 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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- Laurie A. Bankston
- 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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- Mitsutoshi Iimura
- 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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- Martin F. Kagnoff
- 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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- Lars Eckmann
- 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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- Michael Karin
- 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.
抄録
<jats:p> 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 κB (NF-κB) and antibacterial defenses, but CD clinical specimens display elevated NF-κB activity. To illuminate the pathophysiological function of NOD2, we introduced such a variant to the mouse <jats:italic>Nod2</jats:italic> locus. Mutant mice exhibited elevated NF-κB activation in response to MDP and more efficient processing and secretion of the cytokine interleukin-1β (IL-1β). These effects are linked to increased susceptibility to bacterial-induced intestinal inflammation and identify NOD2 as a positive regulator of NF-κB activation and IL-1β secretion. </jats:p>
収録刊行物
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- Science
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Science 307 (5710), 734-738, 2005-02-04
American Association for the Advancement of Science (AAAS)
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詳細情報 詳細情報について
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- CRID
- 1361699995646496768
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- NII論文ID
- 80017220538
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- ISSN
- 10959203
- 00368075
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