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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 "1.4" provenance.
- large_corpus.bel authoredBy _6 provenance.
- assertion wasDerivedFrom large_corpus.bel provenance.
- assertion wasDerivedFrom _5 provenance.
- assertion hadPrimarySource 12496252 provenance.
- _5 wasQuotedFrom 12496252 provenance.
- _5 value "MyD88-mediated NFkB activation is completely abolished in IRAK deficient I1A cells, Pellino 1-mediated NF?B activation is intact in these cells, indicating that Pellino 1 functions downstream of IRAK. On the other hand, Pellino 1-induced NFkB activation was inhibited by a dominant negative, kinase-inactive TAK1 mutant (TAK1 DN; Official Gene symbol - MAP3K7), indicating that Pellino1 must function upstream of TAK1 (Fig. 4 b). In support of this conclusion, TAK1 can still activate NFkB in C-12, where Pellino 1 expression is greatly knocked down by RNA interference (Fig. 4 c). Taken together, the above results support the hypothesis that the Pellino 1-IRAK-IRAK4-TRAF6 signaling complex functions between the receptor complex (Complex I) and the TAK1 complex (Complex II). " provenance.
- large_corpus.bel rights "Copyright (c) 2011-2012, Selventa. All rights reserved." provenance.