Matches in Nanopublications for { ?s ?p ?o <http://www.tkuhn.ch/bel2nanopub/RAAO5iRt2jl31zFjHRkUG3EoQv1y7pbyikaSG_0-VlX5k#provenance>. }
Showing items 1 to 11 of
11
with 100 items per page.
- _7 label "Selventa" provenance.
- large_corpus.bel rights "Copyright (c) 2011-2012, Selventa. All rights reserved." provenance.
- _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
- _6 wasQuotedFrom 17034424 provenance.
- assertion hadPrimarySource 17034424 provenance.
- large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
- large_corpus.bel description "Approximately 61,000 statements." provenance.
- assertion wasDerivedFrom large_corpus.bel provenance.
- assertion wasDerivedFrom _6 provenance.
- large_corpus.bel authoredBy _7 provenance.
- large_corpus.bel version "20131211" provenance.