INT117221
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Surprisingly, after 24 h, although Nod1 and Nod2 expression increased compared to the 6 h samples, all the studied Nod expression remained low compared to the non-exposed samples (Figure 6B). | |||||||||||||||
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We thus hypothesize that alternative splicing of the two novel isoforms contributes to the upregulation of NOD2 protein levels observed under inflammatory conditions and the high constitutive expression in distinct cell types, i.e. monocytic cells and, possibly, Paneth cells. | |||||||||||||||
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A genetic ablation of Nod2 in mice leads to a distinct defect in cryptdin (? | |||||||||||||||
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To determine to what extent the lipopolysaccharide-induced TNF-alpha production capacity in vivo and ex vivo is determined by polymorphisms in toll-like receptor-4 (TLR4), the TNF-alpha promoter region and Nod2, we screened for two TLR4 polymorphisms, a Nod2 polymorphism and the TNF-alpha promoter polymorphisms. | |||||||||||||||
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B phosphorylation upon PGN-ECndss treatment as well as IL-6 inducibility after UV exposure suggest a functional Nod1/Nod2-initiated NF? | |||||||||||||||
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B phosphorylation upon PGN-ECndss treatment as well as IL-6 inducibility after UV exposure suggest a functional Nod1/Nod2-initiated NF? | |||||||||||||||
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and lipopolysaccharide (LPS) activate NOD2 (CARD15) gene expression in intestinal epithelial cell lines and primary intestinal epithelial cells as well as monocytic HL-60 cells [11,12]. | |||||||||||||||
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Tissue specific constitutive and inducible expression patterns of NOD2 have been described that result from complex regulatory events for which the molecular mechanisms are not yet fully understood.
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Crohn's disease-associated mutations in NOD2 result in defective NF kappa B activation, suggesting that Crohn's disease may represent, in part, a defect in innate immunity [4]. | |||||||||||||||
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