INT103909
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
High constitutive expression of NOD2 has been shown in Paneth cells [37], which represent specialized IECs secreting antimicrobial peptides in the terminal ileum. | |||||||||||||||
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We found clear expressions of TLR2, NOD1, and NOD2 and a faint expression of TLR4 in human dental pulp fibroblasts (HDPF) by RT-PCR and flow cytometry. | |||||||||||||||
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We found that Nod1, Nod2, and NLRX1 were expressed at comparable levels in both cell types with an apparently uniform expression level in the primary corneal cell samples. | |||||||||||||||
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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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In addition to its expression on cells of the monocyte lineage, the NOD2 protein is also expressed on gut epithelial cells. | |||||||||||||||
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Within the exon 1b of the alternative 5'-UTR region of human NOD2, three uORFs with variable lengths were identified upstream of the main ORF located in exon 2. | |||||||||||||||
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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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Of the children with NOD2/CARD15 variants...[32] | |||||||||||||||
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Of the children with NOD2/CARD15 variants...[32] | |||||||||||||||
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As in Crohn's disease, CARD15/NOD2 mutation is believed to be responsible for the granulomatous autoinflammatory reactions probably triggered by microorganisms in BS. | |||||||||||||||
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A strong linkage disequilibrium was found between the NOD2/CARD15 Pro268Ser loci and three other studied loci of NOD2/CARD15. | |||||||||||||||
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A strong linkage disequilibrium was found between the NOD2/CARD15 Pro268Ser loci and three other studied loci of NOD2/CARD15. | |||||||||||||||
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As in Crohn's disease, CARD15/NOD2 mutation is believed to be responsible for the granulomatous autoinflammatory reactions probably triggered by microorganisms in BS. | |||||||||||||||
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OBJECTIVE: To investigate the role of the gene NOD2 in susceptibility to, and clinical manifestations of, ankylosing spondylitis (AS). | |||||||||||||||
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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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Roles of TLR2, TLR4, NOD2, and NOD1 in pulp fibroblasts. | |||||||||||||||
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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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The time-dependent appearance of pIkB after PGN-ECndss treatment implies the presence of functional Nod1 and/or Nod2 proteins in HCE-T cells that are able to recognize the peptidoglycan ligand and trigger the NF? | |||||||||||||||
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A strong linkage disequilibrium was found between the NOD2/CARD15 Pro268Ser loci and three other studied loci of NOD2/CARD15. | |||||||||||||||
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