Nanopublications

Matches in Nanopublications for { ?s ?p ?o <http://www.tkuhn.ch/bel2nanopub/RAMaJTbN02WOjBJmIOXTDzPoqmMyGVAst5F89RxbOsCCw#provenance>. }

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_6 label "Selventa" provenance.
large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
large_corpus.bel description "Approximately 61,000 statements." provenance.
large_corpus.bel version "20131211" provenance.
large_corpus.bel authoredBy _6 provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
assertion wasDerivedFrom _5 provenance.
assertion hadPrimarySource 16718776 provenance.
_5 wasQuotedFrom 16718776 provenance.
_5 value "Lipopolysaccharide (LPS), which is a component of the outer membrane of Gram-negative bacteria including H pylori, is a signalling molecule for the innate immune system and is the main source of infl ammation in Gram-negative infections[55]. LPS targets the transmembranous patternrecognition receptor called toll-like receptor 4 (TLR4), which is expressed on macrophages and monocytes[56]. LPS binding to TLR4 activates signal transduction through MyD88, interleukin-1 receptor associated kinase and TRAF6 to activate the NF-?B and mitogen-activated protein kinase pathways[57-59], which leads to the synthesis and release of infl ammatory cytokines such as IL-1, IL-8 and TNF-?, various chemokines GRO?, IP10, MIG and MIP -1? & ?[60], iNOS[61,62] and antimicrobial peptides providing a critical link to the adaptive immune system[63,64].Induction of infl ammation is an important component in the defence against H pylori. The presence of H pylori leads to the release of mutagenic substances such as metabolites of inducible nitric oxide synthase (iNOS), which is known to promote oncogenesis[65]. Nitric oxide generated by iNOS is converted to reactive nitrogen species, which can exert oncogenic effects including direct DNA and protein damage, inhibition of apoptosis, mutation of DNA and cellular repair functions such as p53 and also promotion of angiogenesis[66]. H pylori infection is also known to induce the expression of pro-infl ammatory Cyclooxygenase enzyme (COX-2)[67-71]. COX-2 expression is normally undetectable in most normal tissues, but is induced rapidly during an inflammatory reaction[72,73]. Cox-2 activity is induced by a variety of mediators including inflammatory cytokines such as TNF-?, interferon-? and IL-1[74]. COX-2 facilitates tumour growth by inhibiting apoptosis, maintaining cell proliferation and stimulating angiogenesis within cancer cells[75-77]." provenance.